A system of practical medicine. By American authors. Vol. 2

by Unknown

PERITONITIS.

BY ALONZO CLARK, M.D., LL.D.

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Italian physicians in the later years of the seventeenth century and in the early ones of the eighteenth had acquired some knowledge of the symptoms of the disease we now call peritonitis, but known to them as inflammation of the intestines. Indeed, it is claimed by some of the admirers of Hippocrates that there are passages in his writings that indicate some knowledge of the disease. But this claim will probably be always received with many doubts as to its validity.

In confirmation of the first statement I will transcribe certain passages from Morgagni's thirty-fifth letter: In inflammation of the intestines "Albertini had observed the pulse to be low and rather weak, such as you will find it to have been in general in the foregoing letter under Nos. 9, 11, 18, and 25." He also observed the abdomen to be tense and hard, the face and eyes to have something unusual in their appearance. "Medical writers, indeed, agree in the tension of the abdomen, but they add many other symptoms, which prove beyond a doubt the intestines to be inflamed; yet they mean that evident inflammation which all may easily ascertain, and not that obscure disorder which we now speak of, and which few suspect" (gangrene of the intestines). "By the same writers it is also supposed that there is an obstinate costiveness and continual vomiting."

Morgagni refers to the assistance rendered by Albertini, Valsala, Van Swieten, Rosa, and others in elucidating this subject. It is singular, considering the clearness of his perception of the symptoms of inflammation of the intestines, that he should be so greatly confused regarding gangrene and sphacelus of the same parts. He looks on these as the result of inflammation, and when the two classes of cases are considered and compared, the result is a contrast and not a resemblance. Yet he supposes that the differences are to be accounted for by the different modes in which the same disease may be developed in different persons.

Another thing obtrudes itself on the attention in these letters: that while a number of post-mortem examinations are reported of those who had died of inflammation of the intestines, of gangrene and sphacelus of the intestines, of hepatic abscess opening into the peritoneal cavity, there is no record of finding in the abdomen anything corresponding to what is now known as the inflammatory effusions from serous membranes.

Sydenham died in 1689. I have searched his works, not for peritonitis, for the word was not in use in his day, but for some account of inflammation of the intestines or of some disease in the description of which symptoms are named that distinguish or belong to peritonitis, and with the single exception of pain the search has been fruitless.

Cullen in 1775 mentions the disease, but says that so little is known about it that he will not attempt a description of it.

Bichat died in 1802 in the thirty-eighth year of his age. I am not able at present to lay my hand on his Pathological Anatomy; I therefore quote from Chomel's article on peritonitis in the Dictionnaire de Médecine to show his claim to important studies regarding that disease: "For a long time peritonitis was confounded under the name of inflammation du bas ventre with inflammations of the abdominal viscera; and it is to Bichat belongs the merit of having proved that inflammation of the peritoneum is a disease distinct, and that it ought to be separated from enteritis, gastritis, etc., as pleurisy is separate from pneumonia. The studies of Gasc and of Laennec soon confirmed the opinion of Bichat, and assured to peritonitis the important place which it ought to occupy in all nosological tables. It has become since then a subject of numerous observations and of interesting researches regarding the causes de sa marche and the lesions it causes."

The references are not given by Chomel, but they are probably these: Laennec, Histoire des Inflammations du Peritoine, 1804; and Gasc, Dictionnaire des Sciences Méd., p. 490, 1809.

Gasc says that the twenty years next preceding his publication witnessed the first stage of the true history of peritonitis. Walther in 1786 had contributed some facts, and S. G. Vogel in 1795, but the rounding off and completing their work was left for Bichat.

Acute Diffuse Peritonitis.

MORBID ANATOMY.—The first thing that strikes the observer in the post-mortem examination of a person who has died of this disease is the tendency of the intestines to protrude through the cut made in the abdominal wall. This is produced by their dilatation generally, both small and large, by gas. No gas, under these circumstances, ever escapes from the peritoneal cavity unless there has been perforation of the alimentary canal somewhere. While the intestines are in this manner dilated, the stomach is small and usually empty.

On the surface of the intestines there will be found a layer of coagulated fibrin, often very thin and delicate, requiring a scraping of the surface of the peritoneum to demonstrate it, but commonly obvious enough, and sometimes quite abundant. This same false membrane can be found on the viscera covered by the peritoneal membrane, on its anterior extension, and most at the point of contact of one coil of the intestine with another. Incorporated with this new membrane or lying under it will often be seen blood-spots, thin, translucent, diffused, and having ill-defined boundaries.

The blood-vessels themselves are not remarkably congested. Here and there may be spots where some redness remains, and the vessels are larger than natural. But the congestion and redness, which analogy leads us to believe belong to the active stages of the disease, have in great degree disappeared after death.

The peritoneal membrane itself has hardly become thickened, certainly not in marked degree, but it has lost its lustrous surface, is, at least in parts, of an opaline color, as if it had absorbed diluted milk, and there is an effusion of serum or slight oedema on its attached surface. Whatever may be the popular opinion regarding the termination of inflammation of the bowels in mortification, whatever the opinion of the older physicians, it is safe to say that gangrene of the peritoneum has never been the result of uncomplicated, diffuse, acute peritonitis. Peritonitis from strangulation of the intestine or analogous causes is of course excepted. But in puerperal peritonitis I have noticed a fact to which I have nowhere seen an allusion. The parietal peritoneum is at two points in the abdomen but loosely attached to the wall. One of these is on the anterior wall, anterior to and a little above the iliac fossa; the other is above and below the kidney on each side of the body. In these parts I have seen the membrane forced off from its attachment to the walls, which with it made a sac containing pus. Such an abscess, if the patient live long enough, would doubtless cause the death of the membrane.

There is in almost every case of peritonitis more or less of serous effusion, commonly not seen at first on opening the abdomen, for it has sunk into the pelvis. It is transparent, of a yellowish hue, and sometimes flocculi of lymph are found in it.

Whether the inflammation of the peritoneum extends to organs covered by it is a question that has been much discussed; but it is admitted that these organs, to a shallow depth on their surface, have an unnatural color; and when it is remembered that the peritoneum is nourished by vessels not exclusively its own, but running along its attached surface, and distributed as well to the surface of the organs it covers, it is easy to admit that to a very limited depth the organs partake of the inflammatory disease. This supposition gives an easy explanation of the constipation which is so prominent a feature among the symptoms of the disease.

The manner in which the false membrane is disposed of in those who recover is an interesting question. Forty or more years ago Vogel described the process by which the new effusion became a living tissue, and the manner in which blood-corpuscles and blood-vessels were formed in it; and another author had found that the time needed to complete this vascularization was twenty days. But now Bauer and most of the German writers inform us that the coagulated fibrin is converted into fatty matter and is absorbed, and that when adhesions occur they result from the coalescence of a new formation of the connective-tissue elements built up into granules. The question, then, arises, Will the chemical constitution of fibrin permit its conversion into oil? If it will, then the further question presents itself, By what chemical action is the change effected within the body? I do not intend to discuss these questions, but propose them by way of expressing some doubt regarding the accuracy of this statement.

I have always supposed that the epithelial layer of the peritoneum was pushed off by the first of the effusions in peritonitis, and that this was one of the causes of the lustreless appearance of the membrane. This opinion I have never attempted to confirm or correct by the microscope. Bauer confounds this idea. He says: "The deposition of fibrin occurs before the endothelium presents any changes. This fibrinous effusion encloses, primarily, hardly any cellular elements, and only a few cast-off endothelial cells are to be found in it. The endothelium itself is swollen and turbid; the cell-body is increased in size; the contents are granular; multiplication of the nuclei is apparent; the cells are, in fact, in active division. In the tissue of the serous membrane itself, soon after the deposition on its surface, an accumulation of indifferent (?) cells takes place, especially around the vessels, so that the spaces between the vessels are thus completely filled up. The fixed connective-tissue corpuscles take part in the inflammatory process."

Delafield says: "If the autopsy is made within a few hours after death, we find the entire peritoneum of a bright-red color from congestion of the blood-vessels; but that is all: there is no fibrin, no serum, no pus; epithelial cells are increased in size and number." For this kind of peritonitis he proposes the term cellular. He finds it in cases of local abscess of the abdominal cavity in which inflammatory action has extended over the whole membrane, and particularly on the omentum also, in the first two days of puerperal peritonitis. "The ordinary form of acute peritonitis is attended with changes in the endothelium and fixed connective tissue, and with the production of serum, fibrin, and pus." He describes the migration of white corpuscles of the blood through the walls of capillaries to become pus-cells, and then says: "Minute examination shows that two distinct sets of changes are going on at the same time: first, a production of fibrin, serum, and pus; second, swelling and multiplication of the endothelial cells. If the inflammation is very intense, the pus and fibrin are most abundant; if milder, the changes in the endothelium are more marked."

I have said above that the epithelium is early washed off by the inflammatory effusions. In opposition—or, perhaps better, in correction—of this idea, Delafield says: "There may be a considerable amount of pus produced, and yet the layer of endothelium remains in place." "If, however, the pus and fibrin are produced in large amounts, the endothelium falls off and leaves the surface of the peritoneum bare." The connective-tissue cells of peritoneum, he says, undergo but little change in the first three days of the inflammation, "but by the seventh day these cells are marked by increase in size and number in all parts of the peritoneum."

Two or three times in my life I have met with a peculiar arrangement of the false membrane and serum of peritoneal inflammation, of which I do not remember to have seen a description. It is this: the serum is enclosed or encysted in bladders, the walls of which are the false membrane. There may be two or three layers of these bladders, one upon another, all more or less flattened, and each holding from two to six ounces of fluid. It would seem that in these cases the inflammatory activity rose and fell in its progress, early reaching the point at which coagulable lymph was effused, then falling to the stage in which serum alone escaped. This serum lifted the false membrane irregularly, so that several pools were formed. After this the inflammation returns to the fibrous exudation stage, and gives to these bladders a floor which blends with the roof at the edges, and thus makes a complete sac. Once more the inflammatory action is changed in its intensity, so that the only effusion is serum; and this serum again raises the new layer of false membrane into bladders—not always or generally in the exact position of the first series. Still again, the inflammation may be so changed as to make a fibrinous flow to this second series of bladders. I am not certain that I have seen a third series of these rare productions. They have doubtless been seen by other persons, and may have been described. I have not been an exhaustive reader on the subject, but I can well understand how they may have been called hydatids on examination of the sacs without looking at the contents. The fluid in the cysts is simply serum, with no echinococcus sacs, and then the number of these inflammatory sacs greatly exceeds the probable number of the fibrous sacs of hydatids.

Pus in large quantity is not often a product of simple acute diffusive peritonitis, although it is frequently found in that form of the disease that attends puerperal fever, septicæmia, or erysipelas. Yet I have seen it a few times. The pus is not generally pure, but is mixed with serum in different proportions, and there will be seen at the same time deposits of lymph attached to the peritoneum or scales of it floating in the fluid effusion, or both. There is reason to believe that in the cases of this class a very large proportion are fatal in the acute stages, but in the cases that live for a few weeks the pus is disposed to collect in pools and become abscesses by adhesions around them at their borders. These abscesses are disposed to find an exit from the body. In one case four abscesses that were found in this way in different parts of the abdominal cavity had each burrowed toward the umbilicus, and were actually discharging their contents at this point when I saw the case. In another case one abscess only was formed, and in four weeks it had perforated the colon. The opening was nearly an inch in diameter.

Kalantarians says, in eight examinations of the solar and hypogastric plexus in persons who had died of acute peritonitis changes which he regards as inflammatory had occurred, with subsequent opaque swelling of the nerve-cells, ultimate fatty degeneration, brown pigmentation, and atrophy. In chronic peritonitis the cells are often converted into amorphous pigment matter, with increase and sclerosis of the ganglionic connective tissue. Still, it is worthy of notice that these changes do not express themselves in symptoms in those that recover.

ETIOLOGY.—Numerous writers have expressed a doubt whether a spontaneous acute peritonitis ever occurs, or if it is ever primary its occurrence in this way is very rare. Habershon¹ has presented the case with more apparent force than any other writer. He studied the record of five hundred autopsies of peritonitis made at Guy's Hospital during twenty-five years, but he "cannot find a single case thoroughly detailed where the disease could be correctly regarded as existing solely in the peritoneal serous membrane."

¹ Medico-Chirurgical Trans., vol. xliii. p. 5.

This statement must be received with some caution. In twenty-five years the records were probably made by a number of different persons, and persons of varying views and varying capacity and judgment. It is possible that the quotation may embrace some of the changes already referred to as the consequences of peritonitis. It does embrace the cases "when inflammation of the serous membrane occurs in the course of albuminuria, pyæmia, puerperal fever, erysipelas, etc." It also includes "peritonitis caused by general nutritive changes in the system," as seen "in struma, cancer, etc.," "comprising also those cases in which the circulation of the peritoneum has been so altered by continued hyperæmia (modifying its state of growth) that very slight existing causes suffice to excite mischief, as in peritonitis with cirrhosis, disease of the heart, etc."

With these explanations the statement differs widely from what it would seem to mean without them. It is far from saying that peritonitis always follows some abdominal lesion and is caused by that lesion.

Habershon's paper was published twenty-three years ago, and during all these years the curative treatment of peritonitis, to which the paper itself gave currency, has enabled us to study our cases after recovery as well as before the sickness, and it can hardly be doubted that a much larger proportion of the cases are primary and idiopathic than either Louis or Habershon found reason to admit. That a large number are produced by preceding lesions and constitutional conditions no one will be likely to doubt.

Among the 500 post-mortem examinations of peritonitis reported by Habershon, he found preceding disease or injury recognizable in the abdominal cavity in 261. The following is his table, viz.:

From hernia, of which 19 were internal obstruction	102
From injuries or operations	35
From perforation of the stomach, ileum, cæcum and appendix, colon, etc. (other 13 mentioned with hernia, or with cæcal disease)	43
And leading to fecal abscess (2 otherwise mentioned)	17
From typhoid ulceration without perforation	5
From disease or operation on bladder and pelvis, viscera, etc.	42
From disease of the liver and gall-bladder	11
From acute disease of the colon (3 others enumerated with perforation)	3
From disease of the cæcum or appendix (9 others previously mentioned)	3
	261

Habershon says that in the (his) second and third divisions of the cases the causes were as follows:

From Bright's disease	63
From pyæmia, 13; erysipelas, 5; puerperal fever, 10; with pneumonia, 3	31
From strumous disease	70
From cancerous disease	40
From hepatic disease	27
From heart disease	9
	240

I have drawn thus liberally from Habershon's paper because it is the only paper that I know, in any language, founded on the analysis of a large number of cases (for five hundred post-mortem examinations is a large number for a disease no more frequent than peritonitis), in the belief that he dealt with facts and that his conclusions must be of great value. He may differ with other physicians regarding what constitutes strumous disease and in the agency of heart disease. He may have mistaken coincidence for consequence, but the paper bears the marks of honesty and good faith from the beginning to the end.

In Habershon's second division, under which he ranks the cases of peritonitis caused by "a changed condition of the blood," he ascribes 63 to albuminuria. Every physician knows how often meningitis or pericarditis or pleurisy may occur under these circumstances, especially in young persons; but, for myself, I cannot but express surprise at these figures. In one capacity or another I have been connected with large hospitals for forty-eight years, and have seen many cases of albuminuria in private practice, and can recall but few instances in which kidney disease, excepting cancer and other tumors, has terminated in peritonitis. In modification of this statement, however, it is proper to add that the hospital physician cannot know how half the diseases he treats terminate, on account of the American plan of interrupted service, and even less can he know of the mode of death in cases which he sees in consultation. Even with this admission, from my standpoint it is not easy to believe that one-eighth of the cases of peritonitis are caused by albuminuria.

The word pyæmia used by Habershon, it seems to me, ought to be replaced by septicæmia, and it has been by many of the profession. Sédillot many years ago proved that laudable pus injected into the blood-vessels of the dog produced no signs of disease, but that septic pus, so used, was followed by grave symptoms, even death. Among the author's cases thirteen were associated with the septic poison. He also found five which he thinks were independent of erysipelas. One in one hundred is a proportion hardly large enough to establish the relation of cause and effect against the chances of concurrence.

I can make a remark with reference to the inquiry by C. Dubacy in the October number (1881) of the American Journal of Medical Sciences, whether diphtheria produces peritonitis. When diphtheria became epidemic among us in 1860 or 1861 for several years, I saw a great deal of it, but did not recognize any relation between it and peritonitis.

The relations of hernia, injuries, and operations to peritonitis need no commentary.

Perforations of the alimentary canal may require some illustrative statements. These occur most frequently in the vermiform appendix of the cæcum, and are almost invariably caused by some irritating substance imprisoned in its tube. In some cases it is a seed of some fruit, as the orange or lemon; in others, a cherry-pit; in one that I remember it was a small stone, such as is sometimes found in rice; in others, a hard fecal concretion; in one, a child, a singular formation: a strawberry-seed was the centre; around this a layer of fecal matter, around the fecal matter a calcareous layer, on this, again, a fecal layer, and so on to the number of six layers, the external one being calcareous. This body was about one-fourth of an inch in diameter, and may have been years in forming. In this connection I may state, per contra, that I am informed that in a pathological museum in Boston is preserved an appendix that contains, and did contain, a large number of bird-shot, which did no mischief except to enlarge the appendix. This was from the body of a man who had shot and eaten many birds. My observation has led me to the belief that a large proportion of the cases of peritonitis occurring in children are due to perforation of the appendix.

Of the diseases of the liver producing acute diffuse peritonitis, the foremost, I think, is abscess, single or multiple. The different modes in which gall-stones may produce it may be illustrated by the following cases: (1) A lady died of acute peritonitis. At post-mortem examination a large abscess was found, bounded above by the liver, in other directions by adherent intestines; it contained nearly a quart of pus: at the bottom of the sac was a single gall-stone, very large and very black; the gall-bladder was perforated and very much shrunken. The gall-stone had caused an ulceration of the gall-bladder, but none of the intestines, in this respect differing from the process known as painless transit of a gall-stone. So the calculus caused the abscess, and the abscess caused the general peritonitis. (2) A lady between fifty and sixty years of age had an attack of gall-stone pains; she had had them before. In a few hours symptoms of peritonitis were manifest, and she died. The post-mortem examination showed the ductus cysticus was ulcerated and perforated. Two gall-stones of large size had been formed in the gall-bladder, and had been pushed forward into the duct about halfway to the common duct, leaving it enlarged as they advanced. The foremost one had caused an ulcer on the anterior or lower side of the duct, and bile had escaped, staining all the right half of the abdominal cavity, and throughout this half only the parts were covered with false membrane and stained with bile.

These cases are not so very uncommon. John Freeland of Antigua had a patient, a colored woman sixty-five years of age, who had been suffering from intermittent fever, gastric disorder, and retching. In one of the vomiting spells she experienced great pain, which, being relieved by an opiate, soon returned and was attended by tympanitic and tender abdomen. Death occurred in collapse about eight hours later. The cavity of the abdomen was found filled with blood and bile, the intestines inflamed and gangrenous in spots, and there was general peritonitis. The gall-bladder was empty; the hepatic duct was lacerated, and contained pouches in which gall-stones were encysted. One of these bags was lacerated. This laceration was surrounded by evidences of recent inflammation, and caused the general peritonitis.²

² The Medical Record, Dec. 9, 1882.

The perforations of the stomach which I have seen have been attended by little inflammation of the peritoneum. Death has followed this accident in twenty to thirty-six hours. There has been little pain, little tumefaction of the bowels, little tenderness, but a sense of sinking and a peculiar feeling at the stomach which the patient finds it difficult to describe.

The ulcers of dysentery do at times perforate all the coats of the colon, and yet do not with any uniformity cause general peritonitis; but as the destructive process approaches the outer covering the latter becomes inflamed, and lymph enough is effused to close the opening and prevent the escape of the contents of the intestine; so that, while perforation is not uncommon, I have rarely seen diffuse peritonitis accompanying dysentery.

Habershon reports 5 cases in which incomplete typhoid ulcers of the intestines caused peritonitis, and 15 from the complete perforation. I believe that the physicians of this country and those of France have found the complete perforation much the most common.

I do not remember to have seen fecal accumulation in the intestines produce peritonitis at all general. I did see, years ago, a man of middle age in whom fecal impaction in the ascending colon had caused destruction of all the layers of the abdominal wall on the right side, so that the contents of the intestine were exposed to view in a space of three inches by two. This implies that there had been peritoneal inflammation enough to seal the intestine to the abdominal wall on all the borders of this extraordinary ulcer. The man recovered in about six months, and returned to his business.

The inconsiderable operation of tapping for abdominal and ovarian dropsy has sometimes been followed by acute peritonitis. In the early part of my professional life I met with several such cases, and have witnessed the same from time to time since. These were mostly cases of dropsy from cirrhosis of the liver. Habershon found 5 such cases, and 7 in the tapping of ovarian cysts.

The rupture of ovarian cysts has produced peritonitis, but in a larger number of cases such rupture, even when the result of violence, has not led to inflammation; but the kidney secretion has been greatly augmented and the fluid absorbed, so that the rupture has been beneficial rather than harmful.

Tumors, particularly those of a malignant character, are apt to grow to the surrounding structures by adhesions the result of chronic inflammation, but now and then they provoke an acute attack which becomes general. Benign tumors may, in rare instances, do this. In one case a man died of acute peritonitis, and the examination showed that a tumor noticed before death, a very large serous cyst standing out of the left kidney, downward-forward, was the only lesion that antedated the inflammation.

Infiltration of urine, in any of the several ways in which it can reach the peritoneum, is a cause of peritonitis. Pelvic cellulitis may also be a cause, though twenty or thirty cases in succession may run a favorable course with no secondary lesions; it is still recognized as one of the occasional causes of peritonitis.

Among the rare causes of diffusive peritonitis is perforation of the intestine by lumbricoid worms. In such cases the product of the inflammatory action is apt to be sero-purulent, with but a limited amount of fibrin. E. Marcus reports such a perforation, and it was called by Peris ascaridophagie. The worms were apparently not found in the peritoneal cavity, but in the intestines. The perforation had bloodless edges, which lay quite close upon one another, as if they had been separated by a piercing action of the attenuated extremity of the parasite not eaten through.³

³ N.Y. Med. Journal, Jan. 27, 1883.

Lusk finds that certain vaginal injections excite a local peritonitis. Sentey gives the details of a case in which a midwife undertook to procure an abortion by the douche. She used a tube that was large with a spreading mouth or opening, which probably received the neck of the uterus in such a way as to prevent the return of the water. It was, in consequence, forced into the uterus and through one of the Fallopian tubes into the peritoneal cavity. By this a rapidly-fatal peritonitis was developed. He refers to two other similar cases. It would seem that this mode of procuring abortion can be frightfully misused, however safe it may be in skilful hands.

There is a word still to be said regarding the difference between peritonitis produced by wounds, operations, violence, and internal growths, or what, with a little liberty, may be called traumatic causes, and that which arises spontaneously or without recognizable cause. The first shows a tendency to limit itself to the immediate neighborhood of the injury, and more frequently does not become general; while the latter spreads pretty quickly over the whole extent of the peritoneum.

SYMPTOMS.—There is, perhaps, no grave disease whose symptomatology is more easily interpreted, in which the diagnosis is more easily made, than the average case of acute diffuse peritonitis. Yet there are obscure cases which it is difficult to recognize.

In a well-marked case the first symptom is pain. Chomel and even some later writers believe that chill precedes the pain, but to the best of my recollection it has not generally so occurred to me; and the question arises, Have they kept the symptoms of puerperal peritonitis separated from those of simple peritonitis?

The pain is first felt in a somewhat limited space in the abdomen, and pretty rapidly spreads, so that it is soon felt in every part of the bowels. It may remain greatest in the part where it first began, but there are many exceptions to this statement. As the disease advances the pain and tenderness become more marked, and the patient will try to diminish the tension of the abdominal walls by lying on his back and by bending the hip- and knee-joints, often also for the additional purpose of lifting the bedclothes from his abdomen. Often the patient will resist the physician's movement to examine his bowel with the hand. In the last few hours of life the pain ceases.

The pulse in its frequency follows the advances in the disease. At the onset it is not much accelerated, but in two or three hours it may reach 100 to 120 in the minute. Besides becoming more frequent, it becomes smaller in volume and more tense. Toward the end of a fatal case it may reach 140 to 160 in the minute and be very small.

In the early hours of peritonitis the bowels begin to swell, and percussion shows that the swelling is caused by gaseous accumulation. This increases as the disease goes on, so that in some the bowels become greatly distended—so much, indeed, as to diminish the thoracic space and interfere with the respiration. As the disease advances the tympanitic resonance may give place to dulness on percussion on the sides and lower part of the abdomen. This is due to fluid effusion.

Before the introduction of opium in the treatment of peritonitis the green vomit was a marked feature of the disease. It occurs in other conditions, but rarely, and its occurrence in this disease was so common that it was regarded as almost diagnostic. The fluid vomited is of a spinach-green color, and the color is probably derived from the bile; at least, I have examined it repeatedly for the blood-elements, and have not found them. In these days this symptom of peritonitis is not often observed.

Constipation is absolute in uncomplicated peritonitis of ordinary severity, and I believe is caused by a temporary paralysis of the muscular layer of the intestine. It has already been stated that the blood-supply of the peritoneum is through vessels whose capillaries are shared by that membrane and the tissues which it covers. Inflammatory action in the peritoneum of average severity would naturally extend to this muscular layer and render it inactive. When the inflammation abates it recovers its contractile power. Thus, the intestines become entirely insensitive to cathartic medicines. This fact is not observed in puerperal peritonitis, probably because the large share which the uterus takes of the disease may act, in some degree, as a derivative; and then, so far as I know, the muscular layer of the intestines does not undergo the change of color and appearance in the latter disease that has been observed in the former. This obstinate constipation has been noticed from the first discovery of the disease, and during forty years in the first part of this century many physicians believed that if they could overcome it their patients would recover. The present interpretation of this conviction is that if catharsis, which was very rarely effected, did precede recovery, the disease was not of a grave type—if, indeed, it was peritonitis at all.

Sometimes peritonitis occurs in the course of a diarrhoea; then the constipation is not at once established, but the symptoms of the two diseases concur for one or two days, when the diarrhoea ceases.

Abdominal respiration ceases when peritonitis is established, either because the movements of the diaphragm produce pain or because the diaphragm is partly paralyzed, as is the muscle of the intestines. Then the gaseous distension of the bowels obstructs the action of this muscle. As a clinical fact it is important, and has often helped me in a diagnosis. Another kindred fact is that all the indications of peristaltic action cease. I have a great many times placed my hand on the abdomen and patiently waited for a sensation that would be evidence of intestinal movements, but did not discover any—have placed my ear on the surface of the abdomen, and have long listened for the gurgling which is so constant in healthy bowels, and have listened in vain. In this respect my observations differ from those of Battey, who reports that he has heard the friction of the newly-made false membrane in respiration, while I concur with him in the statement that the sensation of friction can be felt by pressure of the ends of the fingers into the abdominal wall so as to produce indentation. It should be said regarding the friction sound in respiration that Battey has the support of Chomel, and he in his turn quotes Barth and Roger; so that there may be in this sign more than I have thus far found. (See case hereafter related.)

The temperature of the body is not, considering the extent of membrane involved, remarkably high. I have recently attended a most carefully-observed case in which the temperature never rose above 104° F. It falls below the temperature of health as the disease approaches a fatal termination.

From the time this disease was recognized as a separate and distinct affection the countenance has fixed the attention of writers. The face is pale and bloodless and the features pinched, and the general expression is one of anxiety and suffering. I do not remember to have seen a flushed face in peritonitis, although the degree of paleness differs in different patients.

The mind is almost always clear, unless disturbed by the medicines used in the treatment. Yet cases are recorded in which a mild, and still more rarely a violent, delirium has been noticed. Subsultus tendinum, and even convulsions, have been witnessed, but whether these symptoms belong to the peritonitis or to an accompanying uræmia has not received the attention of those who have witnessed them.

The urine is usually scanty and high-colored, but it does not often contain either albumen or casts. This statement is presumably untrue of the cases in which Bright's disease preceded the peritonitis and is supposed to be the cause of it—a variety of the disease with which I have already declared my scanty acquaintance. The urine is often voided with difficulty, and sometimes retained, so that resort to a catheter becomes necessary.

The symptoms of this disease are not invariable. In one case the inflation of the bowels is only enough to be perceptible; in another, as I have said, it becomes a distressing symptom, while in most the bowels are obstinately constipated. A case may now and then occur in which evacuations can be procured by cathartics. Pain is regarded by all physicians as the most constant symptom, and it has existed in every case that I have seen, or at least tenderness; but the late Griscom stated to me that a man once came to his office for advice in whom he suspected peritonitis; but the man asserted that he had no pain, and the doctor placed his fist on the abdominal wall and pushed backward till he was resisted by the spinal column, the man asserting that the pressure did not hurt him; yet he died the next day, the doctor declared, of peritonitis. This may be credible in view of the fact that absence of pain in puerperal peritonitis is not very uncommon. The green vomit, which was expected in all cases forty years ago, for the most part, as I have intimated, disappears under the opium treatment. There are persons in whom peritonitis does not accelerate the pulse beyond 100 beats in the minute. The pain, in rare cases, remits and recurs with some degree of regularity, in this respect resembling intestinal colic. Andral reports such a case; I have also witnessed it.

MORTALITY.—Up to the time when the opium treatment was adopted, peritonitis was a fearful word; a large proportion of those attacked by it died of it. In 1832, I began to visit hospitals as a medical student, and for eight years, at home or abroad, was almost a daily attendant. The number of recoveries of those that I saw in that time can be counted on the fingers of one hand. This may be regarded as its natural mortality, for the treatment of that day seemed to exercise little or no control over it. (Farther on this matter will be referred to again.)

DURATION.—Chomel believed that the disease might prove fatal in eighteen hours, while he regards its average duration as seven or eight days. I very much doubt whether peritonitis, not caused by perforation, violence, or surgical operation, was ever fatal in eighteen hours. I do not remember any case of shorter duration than two or three days. Then, on the other hand, the period of seven or eight days in the fatal cases appears to me too long. In the early part of my professional life I remember to have looked for death in three or four days. At present, in the fatal cases, life is prolonged to double or more than double that time. In the majority of those that recover at present the duration of the symptoms is from two days to a week; in a few they have continued fourteen days; and lately I have assisted in the treatment of a case in which there was little amelioration for forty days, and yet the peritonitis was cured.

DIAGNOSIS.—When the symptoms are fully developed there are few diseases that are more easily recognized. It is when these symptoms are slowly or irregularly manifested, or when some other disease which may account for many of the symptoms occurs with it or precedes it, that there should be any real difficulty. It is customary to regard the danger of confounding the transit of a renal or hepatic calculus with peritonitis as worthy of comment. But if the reader will turn to the articles in this work which relate to these topics, he will find the symptoms so widely different from those enumerated in this article as belonging to peritonitis that he will be surprised that this item in the diagnosis should have occupied so much room.

In a case already referred to, in which peritonitis followed gall-stone pains, the transition was so marked by the rapid acceleration of the pulse and swelling of the abdomen that each of the three physicians in attendance at once appreciated the significance of the change. A physician who resided in the country called on me to report his own case. He had a little before had a very painful affection of the abdomen which continued for three days. The pain was paroxysmal, confined to the region of the liver, back and front, for one day; after that there was some tenderness over most of the abdomen, but no tympanitis. His pulse became frequent and his temperature advanced to 103°. His physicians believed that these symptoms justified them in treating him for peritonitis. Yet his position in bed was constantly changed, and no one attitude long continued—a restlessness which never occurs in peritonitis, but is common in calculus transits. Add to this the absence of gaseous distension and of the green vomit, the paroxysmal character of the pain (though I remember one case in which peritoneal pain increased and diminished somewhat regularly, but only one), and, finally, the sudden cessation of the pain, such as often happens in calculus transit when the calculus passes into the intestine,—it is plain that his sufferings were caused by a gall-stone. The elevation of temperature was the result of a long-continued worry of the nervous system, and the abdominal tenderness came from the many times repeated contraction of the abdominal muscles which occurs in hepatic colic. And then, to make the diagnosis more complete, this gentleman, after twelve or fourteen hours of pain, became jaundiced—in the end very much so. There was no absolute constipation, and the stools were of the color of clay from the absence of bile.

The points of difference between renal colic and peritonitis are even better defined and easier recognized than those between it and hepatic colic.

In intestinal colic there may be some inflation of the bowels, and if it continues a day or two there may be some tenderness; but it is for the most part distinguished from peritonitis by the intermittent or remittent character of the pain, by its greater severity while it lasts, by its courting, rather than repulsing, pressure, by the moderate acceleration of the pulse, by no or only slight elevation of temperature (exception being made for long continuance), by the absence of the green vomit, by the absence of the fixed position of peritonitis, etc.

There does not seem to me any need of spending time to distinguish gastritis or enteritis or neuralgia from peritonitis, their symptoms are so wholly different; and if, as is said, the mucous inflammation can penetrate all the coats of the stomach or intestine, and so cause inflammation of the peritoneal layer, that is peritonitis, and will be distinguished by the proper symptoms of peritonitis.

TREATMENT.—Chomel⁴ says: "If general peritonitis is intense, it should be attacked by the most powerful therapeutic agents. One should immediately prescribe a large bleeding from the arm—from 500 to 600 grammes, for example—and repeat according to the need once or even twice in the first twenty-four hours; apply to the abdomen, and particularly to the part of it where the pain was first felt, leeches in large number—fifty, even a hundred—as the violence of the disease may demand and the strength of the patient will permit." He recommends baths, presumably tepid, and describes an apparatus by which the patient can be put into the bath and lifted out of it without pain; prescribes a fixed posture, gentle laxatives, mercurial frictions, blisters; conditionally and doubtfully, paracentesis, emetics under certain circumstances—musk, etc. under others. In the treatment of general peritonitis there is no reference to opium. The word does not occur, but it does in the treatment of peritonitis following perforation. In this condition he would, among other things, give opium à haute dose, but he does not prescribe any repetition or give any details. It is probable that the idea was obtained from Graves, whose first use of opium in this accident was in 1821, although its first publication appears to have been by Stokes in 1832.

⁴ Dictionnaire de Médecine, 1841.

Wardell,⁵ who has written the latest treatise on the disease we are considering, relies greatly on bloodletting, but falls short of Chomel in the quantity of blood he would take—would bleed, not to withdraw a certain number of ounces, but to produce certain effects. The venesection is to be followed by the application of leeches—twenty, thirty, or forty—to the abdomen; after this turpentine applications to the bowels. After depletion, he says, opium should be given at once: "two or three grains may be given in urgent cases." Vesication he calls "another of our aids." He disapproves of cathartics, but when there is accumulation in the colon would use injections. "Opium in the asthenic form is the chief agent, and Graves and Stokes were among the first physicians who gave it very largely." "Two or three grains may at first be prescribed, and a grain every four or three, or even two, hours afterward." "In perforation there is sometimes great toleration of the drug. Murchison has known so large a quantity as sixty grains to be given in three days with impunity." Mercurials, he thinks, are of doubtful efficacy. In the paragraph devoted to the treatment of puerperal peritonitis the word opium does not occur, and it is only by a very doubtful inference that we can assume that he would ever use it. Chomel makes no allusion to the use of opium in the same disease.

⁵ Reynolds's System of Medicine.

For two years (1834-36) I was connected with the New York Hospital as house-physician or in positions by which that office is reached. The treatment of acute diffuse peritonitis then and there was formulated as follows: First, a full bleeding from the arm, commonly sixteen ounces, then a dozen or more leeches to the abdomen; following this, another bleeding or not, in the discretion of the physician. Meantime, the patient would take half a grain to a grain of calomel every two hours, with a little opium "to prevent the calomel acting on the bowels," of which there was no danger, in truth. Mercurial inunction was used at the same time. The belief was that after depletion the most important thing was "to establish mercurial action in the system;" in other words, "to diminish the plasticity of the blood." Under this plan I saw one recovery in these two years.

In 1840, I went to Vermont to give a course of lectures in the Vermont Medical College, and while there was called by the physicians to see with them several cases of peritonitis. I found that they were treating the disease on the Armstrong plan; that is, bleeding freely, and then administering a full dose of opium, as they said, "to prolong the effects of the bleeding." In most cases there was a second bleeding and a second administration of opium. Leeches were also used, and irritating applications to the abdomen, and in some cases purges. I found they were getting better results than we were in New York, and I studied their cases as closely as I could, and reached the conclusion that opium was the curative agent, and that it would be safe to omit the abstraction of blood. This conviction grew in strength with every new case, and I saw, with different physicians, several cases, the disease being more prevalent among the mountains there than in the city—at least that year. The idea then formed was that to establish the narcotic effects of opium within safe limits, and continue them by repeated administration of the drug, would cure uncomplicated peritonitis—that a kind of saturation of the system with opium would be inconsistent with the progress of the inflammation, and would subdue it. There was no theory to build the treatment on, and no explanation of the action of the drug in my mind. What I saw of the action of two full doses of opium was the only foundation for the idea. I had in the course of two years after those observations in Vermont 9 cases of general acute peritonitis, 8 of which were cured. All these were reported in succession, as they occurred, to the medical societies and in my college lectures. The plan was adopted by many members of these societies and by others with whom I had opportunity of conversing on the subject, so that soon there were several—I may say many—workers in the field; and in all instances where the practitioner had the courage to carry out the treatment favorable reports were returned. Not that every case of peritonitis was cured, but the recoveries generally exceeded those that followed any other plan ever before used. No physician tried it with a proper understanding of its details, and with courage to execute them, who if living does not practise it to-day.

The treatment of puerperal peritonitis is not allotted to me, and I am very reluctent to encroach in any degree on the province of the very competent and highly-esteemed gentleman to whom that disease was assigned. But the history of the opium treatment is very incomplete without the statement I am about to make, and I trust to his generosity to forgive this encroachment; and all the more confidently because he was not at the time acquainted with the manner in which opium was first introduced into the treatment of puerperal fever.

After the curative action of the drug was demonstrated in general peritonitis, I was anxious to try it in puerperal fever, of which peritonitis forms a part. But I had no hospital and no obstetrical practice. In 1847, I was appointed one of the physicians to Bellevue Hospital, to which an obstetrical department was attached. After one or two years a single case occurred and was sent to my division. I gave her 100 grains of opium in four days, with more or less of calomel—I have forgotten how much. She recovered, but after the symptoms of puerperal fever passed away she had secondary abscesses of the lungs. These kept her ill for several weeks. At length her recovery was complete.

In 1840 there was a very fatal visitation of puerperal fever in this hospital, and on invitation of Vaché, who then had charge of the whole institution, I was a daily visitor and took notes of all the cases. It was from these notes that Vaché compiled his report of the epidemic published in the Medical and Surgical Journal. The disease was fearfully fatal, although every known mode of treatment was tried in different cases, including Brenan's plan by turpentine, but all, with one or two exceptions, with the same result. At this time the opium plan was on its trial, and I had not acquired a confidence in it that authorized me to try it in these cases. The time for it came in 1851. Then a sudden, vigorous attack occurred. One woman was sent to me in whom the disease was well advanced. I instructed my house-physician not how much opium to give, but what effects to produce by it. I found this woman dying the next day, and that she had taken only three grains of opium in three doses. In three or four days seven cases were sent me from the lying-in wards. One was returned for error in diagnosis, and six put under treatment. Having found that prudence in my house-physician was so much more conspicuous than courage, another house-officer, who combined them both, was selected to be in almost constant attendance. The instruction I gave him was in these words: "I want you to narcotize those women to within an inch of their lives." He did it, and saved every one of them. This gentleman is now known over the whole land as a learned and distinguished surgeon. I feel called upon to give his name in this connection, that he may be a witness to the facts I state, and for the admiration with which his nerve and prudence impressed me. One of these patients took first two grains, then three grains, then four, and so on till she took twelve grains of opium at a dose, the intervals being two hours. The state into which the patient was to be brought I have denominated a state of semi-narcotism. The quantity of the drug necessary to produce this state varied surprisingly in different persons. One of these women was pretty fully narcotized by four grains every two hours. She was watched with anxiety; restoratives were kept in readiness, but nothing was done but to suspend the administration of the medicine and to wait. In seven hours the consciousness was fully restored, and the improvement in her condition was wonderful. The disease seemed to be cured. But in a few hours more the symptoms recurred, and the same medicine was again given in three-grain doses, and again narcotism was produced. Taught by the experience of the day before, we waited, and when she recovered from this second narcotism her disease was completely cured. She took no more medicine of any sort. This case was very instructive, as it taught me that over certain cases of puerperal fever opium has absolute control.

From the time here referred to, so long as the obstetrical service was maintained at Bellevue Hospital, a large proportion of cases of this fever, as they occurred, were sent to my wards, and in all these years I have not lost faith in opium. This statement, however, requires an explanation. Puerperal fever is a compound disease. Its great inflammatory lesions are found in the uterus and its appendages and in the peritoneum. When the inflammation of the uterus is the dominant lesion, and is purulent, opium has little or perhaps no control over its fatality; but in the cases in which peritonitis is the ruling lesion, if begun early, it will show its power. In this connection I will only add that in private practice the drug has been perhaps more curative than in the hospital. I have seen many cases in consultation, and a decided majority have recovered. In some instances the patient has fallen into a pleasant sleep, only broken by some administration, and ending with her recovery. In one instance a very eminent physician had undertaken to treat a case by the opium plan, but he had administered the drug so timidly that for fourteen days he had done no more than hold the disease in check. After trial, I found that I could not induce him to give the drug in my way, and I asked him to give me sole charge of the patient for twenty-four hours. To this he assented, remarking, "If you cure her, doctor, I will have it announced to the profession that she was the sickest person I ever saw get well." In half the time allowed me I was able to establish the opium symptoms as given farther on, and the lady slowly recovered.

The treatment of any form of peritonitis by opium permits the use of the drug itself, or of any extract or preparation of it which contains its narcotic qualities, but it is wise to persevere with that one first chosen unless there is strong reason for a change. This caution is based on the fact that we cannot change from one to another and be certain to obtain the same drug activity. For example, we begin with laudanum, and find what it will do. We cannot take in its place the sulphate of morphia with the certainty that we can so graduate it as to get precisely the same effects. Then the quantity which will be effectual in one case may be quite inadequate for the next. The tolerance of opium in different persons varies remarkably, and probably the disease itself increases the tolerance in all. This will be illustrated by some of the details of this paper.

The drug symptoms to be produced are as follows: Subsidence or marked diminution of the pain; some or considerable tendency to sleep; contraction of the pupils; reduction of the breathing to twelve respirations in the minute; in the favorable cases a considerable reduction in the frequency of the pulse; a gentle perspiration; an itchy state of skin, or oftener of the nose; absolute inactivity of the bowels, and after a time a subsidence of the tumor and tenderness in them; some suffusion of the eyes.

Of these several signs of opiumism there is none more easily observed and none more valuable than the frequency of the respiration; and while the physician aims to reduce it to twelve in a minute, there are chances that he will see it fall to something below that. I have often counted it at seven, and in perhaps two cases it fell to seven in two minutes; and yet these cases of marked oppression from opium all recovered. In the cases in which the respiration has fallen so low there has been considerable obtuseness of the mind; but in no case except in the hospital patient already referred to have I seen unconsciousness. Then the sleepiness, so long as the patient is easily awakened, is wholly within the limits of safety.

As to the quantity of opium to be given, I have known two grains every two hours do the work, and in other cases many times this quantity was necessary to produce this condition of semi-narcotism. The plan is to begin with a dose that is safe—say two or three grains of opium or its equivalent of sulphate of morphia—and in two hours notice its effects. If any of the opium symptoms have appeared, repeat the dose; if none, increase by one grain, and so on at intervals of two hours till the degree of tolerance in the patient is ascertained. After that the case can be treated by a diminished occupation of the physician's time—two or three visits a day. The dose is to be increased if the opium symptoms diminish before the disease yields, but always to be diminished or discontinued if narcotism is approaching. The duration of the treatment will be sometimes no more than two or three days; it may be a week, or even a fortnight, and in one case already mentioned the symptoms persisted mildly for forty days, and then yielded. In this case the medicine used was the sulphate of morphia, and the enormous dose reached by steady and graduated increase was one grain and a quarter every forty minutes in a boy ten years old.

In some puerperal cases the doses have been so large as to require witnesses to make the statement of them credible, and the administration of them criminal had not the effect of each dose been carefully studied and the amount of each measured by the action or inadequate action of the next preceding one.

Here are the doses given a woman who fell sick October 13, 1857; the record was made by C. H. Rawson during the treatment, and was kindly given me two or three years ago: On the first appearance of her disease, while the diagnosis was uncertain, 10 grains of Dover's powder gave her a quiet night. The next day the disease was more manifest, and she took of Magendie's solution (2 grains of sulphate of morphine to a drachm of water) x minims every hour; growing worse, at night she took xxx minims every hour; the next day, xl minims every hour, and no change of symptoms. She took in twenty-four hours 32 grains of sulphate of morphia; slept, but was awakened by the slightest noise. On the fourth day 3¹/3 drachms of the solution, and opium as follows: at 4 P.M., 3 gr.; at 5 P.M., 4 gr.; at 6 P.M., 5 gr.; at 7 P.M., 6 gr., and 6 gr. hourly after 7 P.M. Sleep light. Fifth day, in twenty-six hours took in opium and morphine the equivalent of 208 gr. of opium. The sixth day, 212 gr. of opium; on the seventh day, 221 gr. of opium; on the eighth, 224 gr.; on the ninth, the same quantity; on the tenth, the same; on the eleventh, 247 gr., pulse subsiding; on the twelfth, 261 gr., other symptoms better; on the thirteenth, 144 gr.; fourteenth day, 4 gr. hourly; slept for the first time heavily, all other symptoms improving, bowels moved freely, ate well, tympanites subsiding; fifteenth day, 1 gr. of opium every two hours, and at night the last dose. Recovery was complete. The woman denied the opium habit, and the medicines were tested by the apothecary. Such doses can only find their justification in the demonstrated fact that smaller doses will not produce the degree of narcotism desired.

In Keating's edition of Ramsbotham's Midwifery a case is reported by myself in which a woman, by pretty rapidly increasing doses, reached forty-eight grain doses of opium, with the effect of curing her disease and substituting a temporary active delirium.

A word of caution is probably necessary regarding the use of opium in high doses when peritonitis and Bright's disease coexist. I have already said that I have but scanty personal knowledge of such a concurrence, but in Bright's disease alone I have known a large, non-heroic dose of an opiate fatal. For example: A young man had a felon on his finger, and did not sleep, so great was his pain. His physician prescribed 40 drops of laudanum at bedtime. Not sleeping on this, he took another portion of 40 drops, and in the morning he was found in a comatose condition, and in the course of the day he died. A post-mortem examination revealed Bright's disease, which was not before suspected. A woman took half a grain of the sulphate of morphine—for what reason I do not know. I was called to see her when she was in a semi-comatose state. The time between my seeing her and that of taking the morphine was fourteen or fifteen hours; its removal from the body was therefore hopeless. Her limbs were swollen with oedema, and the urine contained albumen and casts. Although the usual means of opposing the poisonous effects of opium were resorted to, they were of little use, and the patient died in the course of the day. These are selected from a considerable number of similar cases that show a similarity in their action on the brain of opium and urea. It seems that opium precipitates the uræmic coma, yet the coma produced by these agents combined is not so profound as that produced by opium alone. There is in it some movement of the limbs or body or some imperfect utterances, yet it seems to be more fatal than the coma of opium unaided. Notwithstanding all this, I have met with several cases of cardiac disease combined with Bright's—perhaps I should say many—in which half a grain of morphia sulphate has been taken every night to procure sleep with only beneficial results. This has been observed several times when physicians have been the patients.

These facts are stated to show the hesitation and prudence that should control the administration of opium when there is urea in the blood, whether there is peritonitis or not; but a case in which one form of Bright's disease preceded, and perhaps caused, peritonitis will be more instructive: A gentleman sixty-eight years of age was attacked by peritonitis on Thursday evening. There was a moderate chill at the onset (this being one of the few cases in which I have witnessed this occurrence). The diagnosis was then uncertain, and he took quieting doses of Dover's powder, which gave him sleep. The next day the diagnosis was easily made. The urine was examined for albumen, and none found. It was, however, scanty. He took only six-eighths of a grain of sulphate of morphine in the first twenty hours. It was then increased, so that in the next twenty-four hours he took two grains of the sulphate in divided doses—a quantity which has been greatly exceeded in hundreds of cases with the best results; but in this case coma was the result. At 10 A.M. on Sunday he was comatose, but not profoundly; he could be aroused. The breaths were five in the minute, the pulse increasing in frequency; secretion of urine next to none. The galvanic battery was used. After seven hours, while the respiration was growing more natural, the pulse grew more frequent and the stupor increased. At 8.30 P.M. the breathing was fifteen in the minute, and full and perfectly easy, but the pulse was running at 140, and the coma unbroken, and the pupils of good size. The effects of the opiate had passed off, but those of uræmia were profound. He died at 11 P.M. After the alarming symptoms occurred we tried to procure another specimen of the urine for fuller examination, but could not. It was only after his death that we procured the evidences that he had shown symptoms of contracted kidney for months. The urine contained no albumen at the time of our examination, as very often happens in that disease.

Regarding other points in the opium treatment there is little to be said. Purgatives are entirely inadmissible. The bowels should be left entirely at rest till they recover their muscular tone; then they will expel first the gas, and then the feces; or if, after the inflammation is subdued, they do not move of their own accord, injections are admissible. I have often left the bowels absolutely inactive for fourteen days without any recognizable consequences. If I meet a physician who believes that leeches are essential, I yield him his point, but never advise them. I do this because a moderate bloodletting will do no harm, and little if any good. The same rule I apply to irritating applications to the surface of the abdomen. Mercurials, I think, are harmful, and therefore I object to them. As to food, it should be milk, fresh eggs beaten up with water and pleasantly flavored, peptones, etc. selected from among those that leave no refuse.

The testimony of physicians who have adopted this plan within my own circle is unanimously in favor of it. B. R. Palmer of Woodstock, Vt., afterward of Louisville, Ky., who was the first to test it, told me after a few years' trial that he used to dread peritonitis as he would dread the plague, but with opium in his pocket he met it cheerfully and hopefully, as he did a pneumonia. Chalmers of New York, who is known by many readers of this article, has a very extensive practice, and he told me lately that he had not had a fatal case of peritonitis in twenty-two years. He embraced the plan early.

Now, how did this treatment originate? From whom did the profession adopt it? In 1836-37, I visited daily the hospitals of London, Edinburgh, and Paris, was in frequent intercourse with the physicians of those cities, and never saw a patient anywhere treated by opium, and never heard the least allusion to it. I can safely appeal to any physician who was familiar with the history of the profession before the year 1840, or for two or three years later perhaps, to inquire whether anything was generally known regarding this treatment of peritonitis, or whether he himself ever heard of it. Let the inquiry be made of Willard Parker of New York or Alfred Stillé of Philadelphia—men of a degree of intelligence and learning that has made them leaders in the profession—and of all the profession at that time. I venture to assume that they were as ignorant as I was of what Graves and Stokes had done.

The following fact is significant: In 1843, Graves published A System of Clinical Medicine, the preface of which is dated January, 1843. In this he says he had previously published essays, lectures, and articles in several medical journals. In this volume he intends, he says, "to revise what I have written, and to compress the whole within the limits of a single volume." There is nothing in the table of contents or explanatory headings of the several chapters of this volume which alludes to treating peritonitis by opium. It is fair to infer that the cases treated in 1823 had made little impression on his mind, and that he did not think his treatment could take rank as a discovery; and yet Stokes had made favorable mention of it eleven years before this publication. Graves, then, did not publish his cases, and the first knowledge which the profession could have of them was through Stokes's paper, published in the Dublin Journal of Medical and Chemical Science, No. 1, in 1832. Perhaps the reason why Stokes's paper produced so little impression on the profession may be found in the fact that first numbers of journals of every sort have few readers. Anyway, it was not till after the opium treatment had attracted much attention in this country that anybody here knew that Graves or Stokes had ever had anything to do with it. Besides, Graves and Stokes had only used opium in cases of perforation, and they had no plan or symptomatic guide in the use of the drug.

There is something new and strange in the following case copied from the Medical Record of May 12, 1883, under the heading, "Operative Measures in Acute Peritonitis:" "Dr. Reibel relates the case of a child, eight years old, suffering from acute idiopathic peritonitis. The disease had resisted all treatment, and the child being, apparently, about to die, it was determined to open the abdomen with a view to removing the fluid and washing out the peritoneal cavity with a solution of carbolic acid. The meteorism was intense. No fluid was found in the abdominal cavity. In prolonging the incision a loop of the intestine was punctured, as evidenced by the escape of gas and intestinal fluid. The wound was washed with carbolic acid and covered with a layer of antiseptic cotton. The following day the little patient was nearly free from pain, and was able to retain a little milk. The temperature had fallen from 104° to 101°, and the tympanitis was almost entirely gone. The (wounded) loop of intestine was adherent to the abdominal wall, and there had been no escape of fluid into the peritoneal cavity. The patient made an excellent recovery."

If the statements of this abstract are true, and the future supports the practice pursued in this case, acute peritonitis is likely to become a surgical rather than a medical disease. Reibel thinks that opening the intestine in the way he did is a better plan than the punctures with the exploring-needle to relieve the patient of the tympanitis. But it will require more facts than one to persuade the profession that this mishap of the scalpel can grow into a rule of practice. (The Record finds this report in the Journal de Médecine de Paris.)

I cannot say that I see the value of a distinction made in 1877 by Gubler between peritonitis and peritonism. By the latter term is meant the total of nervous and other symptoms that arise in the course of peritonitis. Trasour has lately revived this distinction, and thinks it important, and that a light peritonitis may be attended by a grave peritonism. He holds that the distinction is important, because "the treatment of peritonism consists in the administration of alcohol, chloral, and especially of opium in large doses. Of the latter fifteen grains may be given in twenty-four hours." "The symptoms [of peritonism] are produced through the agency of the great sympathetic."⁶

⁶ Med. Record, Aug. 28, 1883.

I cannot say that I have seen great effects follow small causes, but think that, in general, the effects of peritonitis on the pulse, strength, nervous tone, etc. are, to some extent at least, a measure of its severity.

CONSEQUENCES OF PERITONITIS.—These are usually nothing. When recovery takes place it is commonly complete, but cases have been known in which the intestines have been left bound to the abdominal wall and to each other, and so made incapable of their natural action. The results of this are a swollen, tympanitic abdomen and impaction of the bowels, but the general health may be very good. A woman at Bellevue was left in this condition, yet she performed the duties of nurse in one of the wards for some years, and finally disappeared from the institution, and I do not know how it ended with her—probably by the breaking up of the adhesions and a return of the bowels to their natural condition.

In some few cases there remains new tissue, which in time is partly broken up and remains partly attached. In this manner strings and bands of considerable strength can be formed, and into these loops the intestine may pass, so as to form an internal hernia of a very dangerous character. In some bands are formed across the intestine, which by contraction flatten the tube and obstruct the fecal movement. There is reason to believe that such bands and bridles are formed by local inflammation of such imperfect manifestation by symptoms that the patient knows nothing about it. A very striking case illustrating the possible sequence of this inflammation came under my observation early in my professional life: A colored woman about twenty-five years of age gave a very clear history of a peritonitis from the consequences of which she had suffered two years before I saw her. About six months after recovery she began to have constipation and to suffer from small and frequent discharges of urine. The latter gradually grew milky and to have a bad odor; the constipation grew more and more, and at length came to be absolute for many days; then would come a diarrhoea of some hours' continuance, after which she would have a feeling of relief. This was her state when I saw her. She was emaciated, and so feeble as hardly able to leave her bed. She vomited occasionally, and her appetite for food was all gone. The urine was heavily loaded with pus, and was ammoniacal. She died after a few weeks. At post-mortem examination a firm membrane was found strained across the upper strait of the pelvis, wholly separating the abdominal cavity from the pelvic. It looked like a drum-head. The left posterior border was drawn very tensely over the colon where it passed into the pelvic cavity, flattening it down completely and making stricture. To the under or lower surface the fundus of the uterus and the base of the bladder were firmly adherent, and in this way both were suspended. The effect of this unnatural suspension of the inactive uterus did not seem to be noticeable, but with the bladder it was very different: it contained three to four ounces of water, ammoniacal and full of pus, and it could never have emptied itself. The explanation is very simple. During the peritonitis a false membrane was effused on the pelvic viscera in situ. When the period of contraction which is common to all such structures came, the new membrane was separated from the greater part of these two organs, but not from their bases. The firm attachment to the brim of the pelvis did the rest. So unusual a sequel of peritonitis I think deserves a record. I should add there were no adhesions above the pelvis. Such a structure as this, found long after the active symptoms of peritonitis have passed, as also the bands and cords before spoken of, does not give support to the doctrine that the false membranes are broken down into fatty matter, and in this condition absorbed.

The possible remote effects of peritonitis are shown in a case reported by E. A. Mearns to the Medical Record, published Sept. 15, 1883: A young man, aged nineteen, four years after he had had acute general peritonitis was attacked with constipation, which was absolute. He had had before occasional attacks of pain in the bowels and constipation, which were overcome. But this was invincible. He had the train of symptoms usual in intestinal obstruction. There was no fever or tympanitis, and this time but little pain. He lived eight days. There was a tangle and a constriction of the intestines at the middle of the ileum, caused by the contraction and hardening of the effusion of the old peritonitis, and the intestine was very much softened.

H. B. Sands reports in another number of the same journal: "The patient was a man about thirty who had suffered from acute obstruction for a week. No exact diagnosis was made. When the abdomen was opened the intestinal coils were found extremely adherent one to another in consequence of a former peritonitis. A careful search failed to discover the nature or seat of the obstruction. The abdominal wound was closed, and the patient died soon after."

Peritonitis from Perforation.

There is no part of the gastro-intestinal canal that may not, from one cause or another, become the seat of ulceration. The jejunum is the part of the tube long supposed to be an exception to this rule, but even in it one or two observers have found ulcers. These ulcers often exist without distinctive symptoms, and may go on to cicatrization without announcing themselves. In the stomach, however, there are commonly indications which will admit a conjecture of their existence, and perhaps a diagnosis. Sometimes these ulcers penetrate all the tissues of the tube and allow the contents of the intestine to escape into the peritoneal cavity, or they may have destroyed all but the external layer, and some succussion, as in coughing, sneezing, laughing, or perhaps straining at stool, may make the opening complete, with the same results. In these cases it seems to be inevitable that inflammation should follow, unless it has preceded, the complete opening and sealed it up by adhesions. The tendency of such an inflammation is to be local and limited, but when the contents of intestines escape into the peritoneal cavity it usually becomes general. These accidents are usually attended by the sudden development of local pain, by rapid increase in the frequency of the pulse, paleness, and prostration. The perforation of the vermiform appendix is often a partial exception to this statement, for, while the local symptoms are marked, the sympathy of the general system is not so quickly awakened. The same can be said of perityphlitis. The symptoms are often local for some time—a day or more; sometimes subside, as if the disease were cured, and then return in full form. This is produced by the tendency of the inflammation to limit itself to the immediate neighborhood of its cause. Lymph is effused at a short distance from the point of irritation, and seals the parts together, so as to shut in the offending substance; and though this substance may produce pus in contact with intestine or appendix, that fluid is held for a time, as in abscess. It may be permanently held in its new-made sac till it burrows into some near part, as the intestine or bladder, or remain an abscess till opened by Willard Parker's puncture. On the other hand, the contents of this sac may be increased till it breaks bounds and causes extension of the peritoneal inflammation or general peritonitis. In one particular case this process of setting limits and breaking through them occurred in a young lady four times at intervals of from one to two days. When the limiting adhesions were established symptoms would subside, so as to encourage in her physicians the hope, even the expectation, of recovery; but again and again the fire was rekindled, and she died eight days after the first attack. In the greater number of cases the first breaking of the adhesions is followed by full peritonitis, and this often by death.

The perforations of the stomach which I have seen have not been attended by the severe pain described by most authors, but by a sudden prostration of strength and a feeling of disquiet and sinking at the stomach; more of collapse than of inflammation in the symptoms; no tumefaction of the bowels; almost nothing to indicate the nature of the accident, but a sudden new sensation in the bowels, a rapid increase in the frequency of the pulse, it growing small as it increases in rapidity, and a pale and shrunken countenance, and death in from twelve to thirty hours. Then, on inspection, hardly any signs of peritonitis are found. The peritoneal vessels are fuller and the membrane redder than in health, and its surface covered with the thinnest possible film of lymphy exudation, and some serum in the deeper parts of the cavity.

These ulcerations of the stomach are not always fatal by peritonitis. A few instances are recorded in which adhesions of the outer surface of the organ to adjoining organs have taken place, so as to protect the peritoneum almost wholly from the fatal contact with the gastric fluids, and death has occurred in some other way. I have a remarkable specimen illustrating this fact. It was taken from the body of a woman of about middle age who had long had symptoms of dyspepsia, and had from time to time vomited a little blood. It was not difficult to recognize ulcer, but the extent and peculiarities of it could be learned only by inspection. She died suddenly of copious hæmatemesis. On examination an ulcer two and a half to three inches in its several diameters was found, beginning near the pylorus and extending toward the left, which in this large space had destroyed all the coats of the stomach and exposed an inch and more of the right extremity of the pancreas and about the same extent of the liver. The liver and pancreas were both perceptibly eroded when exposed, and in the latter an artery that would admit the head of a large pin was opened. The stomach, outside of this extraordinary ulcer, was strongly attached to the adjacent organs.

The ulcerations of typhoid fever penetrate the intestine about three times in a hundred cases of the fever. This result is reached by the study of a large number of cases, and appears to be pretty generally admitted. The point where this perforation occurs is in the ileum, near the ileo-cæcal valve—within a foot or eighteen inches of it in the great majority of cases, although it has been known to occur seventy-two inches above the valve, and it has been seen very rarely in the cæcum. The fever itself may be either severe or mild. Suddenly severe pain sets in, oftenest in the lower part of the abdomen, and spreads rapidly; the pulse is quickly accelerated and becomes small; and it has been lately stated that in this and other intestinal perforations the gases of the bowels, escaping into the peritoneal cavity, will give resonance to percussion over the lower part of the liver. Fetid gas found in this cavity after death is not without importance; for example, a distinguished Senator at Washington died not long ago of a very painful abdominal disease which his physicians declined to relieve with opium, though the patient pleaded for it. His family physician at home was summoned. Although the distance he had to travel was many hundred miles, he found the patient alive and still suffering. He at once gave morphine for the relief of the pain, but the patient died. Now, this gentleman had diabetes a year or more before his death, recognized by his physician at home and also by myself. While under my observation the urine ceased to contain sugar and its quantity became normal, but soon after this albumen was occasionally found in it. The quantity was generally small, and casts were only found now and then. This new disease was mild, and seemed to be, within certain limits, manageable. He went to Washington under injunction that he was not to let official and professional labors bear with any weight upon him. This last sickness and the death would naturally enough be supposed to be some new phase or consequence of the previous illness. But, while a post-mortem examination was not permitted, the family wished to have the body embalmed. The family physician accompanied the embalmer, and as the latter made a cut through the abdominal walls there was a gush of air laden with fecal odor, and he through this opening saw the intestines covered with false membrane. He satisfied himself that the intestine was not opened. This fetid gas came from the peritoneal cavity. An ulcer had perforated the intestine somewhere, and caused the death. The final disease could be only remotely dependent on the patient's previous illness, if at all. His impaired health may have made the ulcer possible.

All kinds of perforations in the bowels, except those of the stomach, cæcum, and appendix, even the cancerous, have one history and the same symptoms; and if treatment is ever successful in such occurrences it must all be based on one set of rules—absolute rest, no pressure on the bowels, and no movements of the muscles that will aggravate it; food that will be wholly digested and absorbed by the stomach; complete abstinence from cathartic and laxative medicines, and the free administration of opium or morphine. By these means, I fully believe, numbers have already been saved from the fatal consequences of peritonitis caused by perityphlitis and perforation of the vermiform appendix—some under my own observation and others under that of my friends. A boy fourteen years of age was brought to bed by a pain in the right iliac fossa. After a few hours his father, a physician, desired me to see him. There was already a perceptible fulness, with dulness on percussion, in the fossa, and some febrile excitement. I gave a portion of morphine, and promised to call the next morning. In the morning a message came from the father stating that the boy was better and there was no need of further attendance. In the evening I was recalled. The pain had returned, and had spread over most of the bowels. He had general peritonitis. He took tincture of opium, of which I believe the largest dose was 100 drops, reached after three or four days of gradual but steady increase of dose. From that point the patient got better, and the quantity of the medicine was correspondingly reduced. There were a relapse and a repetition of the treatment, and again the disease yielded. During convalescence, about fourteen days from the attack, the boy, after emptying his bladder, was suddenly pressed to continue the discharge. Now he voided what appeared to be blood, two or three tablespoonfuls. It was, however, pus with blood enough to color it. This purulent discharge from the bladder continued for about three weeks, the boy steadily recovering his health. This occurred twenty or more years ago, and that boy is now a well-known physician. Similar cases could be recited.

In 1850, or thereabout, I attended a physician through an attack of typhoid fever. In the third week there was a sudden outbreak of peritonitis. The opium treatment was resorted to, and he recovered, and had good health for twenty years after. Peritonitis occurs rarely in typhoid fever from any other cause than perforation, and its occurrence in this case at this time, when perforation is more likely to occur, renders it probable, at least, that this attack was produced by that cause.

March 3, 1883, autopsy of Wm. Fletcher, age 59, iron-worker. On Friday last, Feb. 23d, he was attacked with pain in the region of the right iliac fossa; it was severe. There was no chill, but little fever, and only slight acceleration of the pulse. His stomach was a good deal disturbed, and the bowels were soon distended with flatus. I saw him on the Tuesday following, with James D. Elliott. The bowels were a good deal swollen and very resonant on percussion; pulse 84. His stomach was still greatly disturbed, so that he retained no food, yet there was no green vomit, but much flatulency. The movements in respiration were particularly noticeable, being nearly or quite as much abdominal as in health. There was a short friction sound in inspiration, but an entire absence of the sound produced by peristaltic action. There was no dulness on percussing over the iliac fossa, and no pain on pressure over any part of the abdomen. I was careful in examining the right fossa, for the first pain was there, and it was severe; but there was no physical sign by which the perforation could be ascertained. Still, my mind dwelt on the probability of perforation, and I expressed my fears to Elliott regarding it. The respiration was of natural frequency. The bowels had not moved for two or three days.

The next day Flint was added to the consultation. The symptoms had changed but little; the pulse was 102; no pain, no tenderness, no peristaltic action; slight friction at one point only; the abdominal respiration was as marked as before. Frequency of respiration, 18; patient sleepy; pupils only slightly contracted. When we were in consultation I again expressed my fear of perforation, but Flint expressed the most decided opinion as to its absence, because there was dulness to percussion over the liver. I had read his paper on the intrusion of gas between the ribs and liver in cases of intestinal perforation, and felt as if I were almost reproved for entertaining the thought without this physical corroboration.

Thursday, March 1st, the stomach had become much more retentive; there were no pain and no tenderness on pressure; pulse 109; no friction sound, no sound of peristaltic action, no dulness on percussion over right iliac fossa, but resonance over the whole abdomen, excepting over the pubes; there the resonance was not clear; over a small space there was dulness; this was ascribed to moderate fulness of the bladder, and, as there had been no difficulty in emptying it, nothing was said of it. The abdominal respiratory movements were the same as before.

Friday morning, at 3 A.M., no marked change had occurred in the symptoms, but from this time onward there was a steady sinking of the vital powers. The pulse grew small and frequent, the hands became cool, the breathing more frequent, and without any sudden change or new symptom he died early in the morning. At the last visit there was no resonance on percussion over the liver.

Autopsy, Saturday, March 3d, 2 P.M. The bowels were distended, as they mostly are in peritonitis, but not extraordinarily. There was now pretty free resonance over the liver. The section to open the abdominal cavity was carefully made, with the aim of ascertaining whether there was air or gas in the peritoneal cavity. When a half-inch opening was made through the peritoneum, gas was forced out through it for some seconds with an unmistakable noise. The bowels were not opened by this cut. The bowels exposed, a very thin film of false membrane was found on all the middle and upper portions of the intestines, with a fringe of injection where the folds came in contact. But two or three inches above the symphysis pubis the section opened a collection of pus which extended downward into the pelvis. Somewhere hereabout—neither of us could say exactly where—was found a lump of fecal matter, not indurated, as large as a marrowfat pea, the intestine still unopened. Search was made for the vermiform appendix. At first it was not recognized on account of its remarkable shortness. It was found, however, pointing directly toward the median line of the body, and was short because a part had been separated from the rest by slough. The end of what remained was marked by a border, one-eighth of an inch deep, of a very dark-green gangrenous color. We did not attempt to measure the quantity of pus. It was six ounces or more. It was completely bounded and shut in by adhesions.

At no time during life was there resonance over the liver, but there was some at the time of post-mortem examination before the bowels were opened, due perhaps to the fact that at death the relaxation of the muscles allowed the gas to rise higher than it did during life. The unusual median position of the abscess is important in accounting for absence of dulness, when it is usually found in slough or ulcer of the vermiform appendix.

"A Fatal Case of Typhlitis without Recognizable Symptoms." Under this title José M. Fisser published a case of inflammation of the vermiform appendix causing general peritonitis in a young woman nineteen years of age. The peculiarities of the case were that the appendix was not perforated, and consequently there was no tumor in the right iliac fossa—that the symptoms were all referred to the epigastrium, without even tenderness in the fossa. She walked the floor and tossed about in bed; the highest temperature was 103°, and the most frequent pulse was 120, and these continued but a short time. Of tympanitis there was none till near death, and then but little. The obscurity in diagnosis led to the publication of the case. The cause of this disease was fecal matter, not very hard, in the appendix.⁷

⁷ Med. Record, Sept. 1, 1883.

As much has been said in this article on the diagnosis of peritonitis, it may be well to introduce a case where that diagnosis was conjectural, and yet quite another state existed. I visited Mrs. H——, when her disease was advanced, twice. My impression was that she had peritonitis, but this opinion was held with grave doubt. After her death, Smith sent me the following record of the autopsy: "Mrs. H—— died Friday evening at ten o'clock; next day, at three in the afternoon, we made an autopsy. No gas or fluid in the peritoneal cavity; the small intestines inflated almost to bursting, with injection of the capillaries. In the left iliac region we at once discovered a portion of the intestine almost black, and on examination found a firm white band encircling and constricting that portion. Upon liberating the gas the intestines collapsed, and the constricted portion was released and easily removed. A further examination showed that two of the epiploic appendages, coming off from the colon above the sigmoid flexure, had united at their extreme points and formed a loop two and a half to three inches long, and through this loop or ring a portion of the ileum had passed, and was there constricted. The constricted intestine was about four feet in length. This examination has been gratifying to me. There was a small quantity of bloody serum in the peritoneal cavity low down in the pelvis. The dark grumous blood that passed the bowels on the second and third days can now be accounted for, and corroborates your remark that the hemorrhage looked like strangulation. This was at your first visit. This must be a new cause of strangulation, and one that we could not anticipate."

There was, before I saw her, a single vomit of a suspicious fluid, but the evidence was not strong enough to enable us to pronounce it stercoraceous. Some of the observers noticed bloody serum in the peritoneal cavity, and perhaps some shreds of lymph, but that was in consequence of the strangulation.

Local Peritonitis.

This may occur anywhere in the broad extent of the peritoneum, and will be more or less limited in different cases, or may be limited for a time, and then become general. It is either acute or chronic. The product of the diseased action may be serum or lymph or pus, or all of them. The cause of this local inflammation is sometimes very obvious, in other cases wholly unknown. The consequences vary all the way from harmlessness to death; the symptoms are as variable as the consequences, making the diagnosis easy in some cases, in others impossible. Some cases in which it was not difficult to recognize it have already been recorded—those caused by perityphlitis and perforation of the vermiform appendix, for example. In such cases the local pain, the swelling, the dulness or resonance on percussion, depending on whether the tumor is made by inflammatory exudation or gas, together with the general symptoms and the history, leave but little ground for doubt regarding the character of the disease. Perhaps one-half the local abscesses which form between the folds of the peritoneum are recognizable during life by the local, associated with the general, symptoms. When situated in the posterior and upper part of the abdominal cavity, the hand gives little, perhaps no, assistance, as in the most widely-known case of abscess that has been recorded in all time. While the physicians were giving to the country hopeful reports day by day, thousands of medical men shook their heads and spoke sadly of the prospects. The illustrious patient was losing rather than gaining strength and flesh, his appetite poor, his digestion poor—a strong man growing helpless—and, above all, a pulse that for months never fell below 100. With an adequate cause of abscess, whether there were chills or not, what else could it be? Thus, in peritoneal abscesses that cannot be felt the general symptoms are of great importance to the diagnosis. When abscesses tend to discharge their contents soon or late—sometimes into the intestine, sometimes into the bladder, sometimes externally: in such cases there is a fair chance. Sometimes they burst into the peritoneum: such cases are almost inevitably fatal; even opium will not cure them. The pus of these abscesses often has the fecal odor, which it acquires by the transmission of the intestinal gases through the intestinal walls. I was attending, with the late James R. Wood, a young lady in whom peritoneal abscess had been recognized. It was anterior to the intestines. In the consultation, while we were discussing the propriety of using the trocar, the mother became alarmed at the odor and appearance of the urine just passed, and summoned the doctors back to the chamber. The abscess had opened into the bladder. The urine contained pus which gave off the fecal odor strongly. This patient recovered. It should be added that these abscesses, as well as those of the convex surface of the liver and those that are post-peritoneal, sometimes pierce the diaphragm and produce empyema, or by previous adhesion of the lung to its upper surface find a way into a bronchial tube, and so the pus is expectorated.

The history of local fibrinous exudations is not as easily told as that of the purulent. We find from time to time, on the peritoneum, bands, patches, or cords of false membrane, which were produced in so quiet a way that we can get no information regarding the time when they were formed, and perhaps the subject of them was not aware that anything was wrong with the bowels till he began to have the symptoms of obstruction. These unnatural structures are formed in great variety. The omentum is found thickened and contracted. The mesentery and mesocolon are seen in a similar condition, causing wrinkling and shortening of the bowels. The spleen has on its surface patches or even plates, or one great plate, of firm fibrinous deposit, often cartilaginous in density, sometimes calcareous; and we can rarely fix the time of these occurrences by any symptoms. It is not always so with the liver. We are acquainted with a perihepatitis which is acute, attended by pain in the right side, a febrile movement, and, if the inflammation reaches the under surface of the organ, by jaundice, and have learned to combat this with cups and opiates, the latter in rather free but not heroic doses, and to expect recovery in a few days. This may leave the liver wholly or partly invested with a layer of false membrane which may have a sequel of importance. Then, again, we find the organ invested with a thick contractile membrane, but cannot learn that the symptoms of perihepatitis have ever occurred. The diseased action which produced this bad investment appears to be analogous to that which not only covers the organ with a thinner coat of similar new tissue, but inlays it everywhere with the same material in cirrhosis. This also is unattended by local pain. The effects that may result from this encasing of the liver in a strong contractile capsule may be illustrated by the following case (the late Buck was the physician): The patient was an unmarried lady of middle age who had consecrated her life to charitable works. In searching for the suffering poor she often had to ascend several flights of stairs. The time came when she found this fatiguing and a tax on her respiration. She observed at the same time that the bowels were enlarged. She called Buck, and he had no difficulty in discovering ascitic fluid. He was surprised, as he knew that her habits were perfectly good, and she had very little the appearance of an invalid. Notwithstanding the proper use of the usual remedies for dropsy, the fluid slowly increased, and at length he was obliged to draw it off. He found it to be a clear, yellowish serum. In the course of about two years she was tapped four times. I saw her, with Buck, after these tappings, when the fluid had again been effused in quantity that half filled the peritoneal cavity. The emaciation was not considerable; there was nothing of the semi-bronzed color of the skin so common in cirrhosis of similar duration; her appetite and digestion were not materially impaired; the temperature was natural; the pulse was increased in frequency only a few beats. The skin over the abdomen was in a soft, natural state, and there was nothing that suggested a hyperæmic or inflammatory dropsy. The liver on percussion appeared to be reduced in size. Taking all things into account, and especially the patient's habits and the absence cancerous cachexia, it seemed probable that the dropsy arose from atrophy of the liver, and that the atrophy was caused by an adventitious capsule of the organ, although the patient had never had symptoms of perihepatitis. From this point the fluid did not increase or diminish, but remained stationary till she died, perhaps two years after, of some other disease. Meanwhile, the lady resumed her favorite charity-work to a limited extent. At the post-mortem examination the capsule was found investing nearly the whole liver, but not materially obstructing the gall-duct. The new membrane was thick and strong, having a thickness of at least one-twentieth of an inch. The remaining liver structure was of natural appearance. The organ was reduced to one-half its natural size. No other cause of dropsy was found.

Chronic Peritonitis.

I have doubted whether any disease deserving this name really exists independent of such low inflammatory action as may arise from the irritations of tumors or heterologous deposits. This statement refers to general not local peritonitis. I have never seen anything that would lead me to believe that acute diffuse peritonitis can be deprived of its acute character and still continue an inflammation. With me it has always been death or cure. I have already referred to a case in which after recovery the bowels were greatly disturbed by tympanitis for years. But this came from adhesions: her general health was good. I have at long intervals met with cases of ascites in which the peritoneal membrane was redder than natural, and in which no obstruction to the portal circulation was discovered. This, however, I have regarded as hyperæmia rather than inflammation.

Bauer,⁸ however, gives to these cases the title latent general peritonitis, especially when after death an abnormal adhesion is found here and there. In the cases that I have seen there was a peculiar state of the surface of the abdomen. The skin there was more or less scaly and dry, but I do not remember whether there were internal adhesions. Bauer regards the diagnosis of this form of disease as difficult, but refers to the constantly present meteorism as well as serous fluid. I have met with three or four instances in which at the time of puberty an abdominal dropsy has rather suddenly occurred, lasting one to three months, and disappearing on the use of diuretics. I have had no reason to attribute this effusion to inflammatory action, except in one case. A lady of extraordinary symmetry and beauty of form, in excellent health, whom I had treated for this disorder twelve years before, applied to know whether there was anything in that disease that would prevent her having children. She had been married seven or eight years, and had not been pregnant. The question then occurred to me, At the time of the dropsy could there have been lymphy exudation that has since confined the ovaries in an unnatural position? The question I could not answer. The treatment which Bauer prefers for his latent peritonitis consists in "painting with iodine, the use of diuretics, and the regulation of diaphoresis by means of Turkish baths."

⁸ Cyclopædia of the Practice, etc., vol. viii. pp. 297-302.

Another form of general chronic peritonitis is, according to Bauer, that which follows acute peritonitis. He quotes several authorities in support of his views. I must draw on him for a description of it, for, as I have said, practically I know nothing about it.

The symptoms of acute peritonitis are all toned down, but do not all disappear. Vomiting occurs occasionally; tenderness is diminished, but is quite perceptible; meteorism diminishes, but fluctuates greatly; appetite is poor or variable; constipation alternates with diarrhoea or is followed by dysentery; now there is a febrile heat, and then the temperature is normal—this fever is most likely to come in the evening; the pulse is frequent and varying; ultimately extreme emaciation and anæmia. The most striking feature of this condition appears to be sacculation of the fluid in the abdomen, wholly or partially; this fluid then is not freely movable, but will give dulness on percussion, which may contrast well with intestinal resonance in its immediate neighborhood. When the tension of the abdominal wall is diminished these sacs can be felt by the hand as uneven tumors. Colicky pains occur, and in a case cited it was at one time very severe, at another only slight. The majority of the cases terminate, after a protracted course, fatally. Recovery may occur by absorption or external evacuation of the fluid. He gives no special treatment.

Bauer makes still another class of cases of chronic peritonitis—those arising in the course of old ascites; he, however, does not make much out of it. He thinks the cases of this kind occur with cardiac and hepatic disease, and particularly with the nutmeg liver. The symptoms, he admits, are neither well defined nor severe, and the anatomical changes consist "in thickening of the serous membrane by a slight deposit of fibrin, slight turbidity of the ascitic fluid, and a few flakes of fibrin suspended in it." He then, strangely, gives, as if they were illustrations of such a disease, two cases in which death by acute peritonitis followed the last of many tappings, in one of which a pool of pus was found encysted in front of the intestines. Both are borrowed.

Probably most practitioners who are in the habit of making post-mortem examinations have seen the flakes of lymph in the ascitic fluid, etc., but the German physicians have been the first, I believe, to regard such cases as belonging to separate forms of disease.

William Pepper has published⁹ a case observed by himself and G. A. Rex which shows non-malignant chronic peritonitis better than any I can recall to mind. The report forms the sequel to the case of the young woman on whom he successfully performed paracentesis of the pericardium.

⁹ Am. Journ. of Med. Sci., April, 1874.

This young woman began to have double pleuritic effusion, and this was soon followed by ascites three and a half months after the operation. From that time the ascites was better or worse, but did not wholly leave her, and became considerable before her death. This was sudden, she having some convulsive movements in extremis. Lesions were found in the thoracic cavity like those discovered in the abdominal, showing, it was believed, a special tendency in this person to plastic exudation on the serous membranes. "The lower part of the abdomen was found occupied by an extensive effusion. The intestines were floated upward. There were few if any signs of inflammation of the intestinal peritoneum, but marked changes were observed in the parietal peritoneum and in the capsules of the liver and spleen. The peritonitis was most marked in the upper segment of the abdomen, while the parietal membrane presented large patches of irregular thickening. No tubercles were found on any part of the peritoneum. The capsules of the liver and spleen were greatly thickened, whitish, opaque, and densely fibrous. The liver was enlarged and heavy, and so tightly bound by its thickened capsule that its shape was somewhat altered.

"The diaphragm, especially that part of it underlying the pericardial sacs, had undergone marked fibroid degeneration. The muscular tissue was much atrophied; many fasciculi had evidently disappeared, while many others were markedly narrowed, some of them shading off to a width of less than ¹/3000 of an inch, and finally disappearing altogether. They retained, however, even in their narrowest dimensions, their transverse striæ."

(It may be remarked, in passing, that this substitution of fibrous for muscular tissue follows the same law that it does in the heart when that organ is the seat of fibrosis or fibrous degeneration. Here it was supposed to be the consequence of a low grade of inflammatory action. Is it when it occurs in the heart?)

In the abdomen these observers found nothing which suggested the possibility of tubercles or any obscure form of cancer. In the pericardium, on the heart side, were found numerous small nodular roughnesses. Irregularities of the pericardial false membrane are so common that nothing but the close and universal adhesions would raise any question of these relations. But tubercles would hardly be here and nowhere else.

Delafield says that one form of the chronic disease is the continuance of his cellular peritonitis. In this, he says, the surface of the omentum is covered with cells which look as if they were derived from the endothelium and connective-tissue cells, although they differ from the normal shape of these. The new cells are for the most part polygonal, of different size, with one or several nuclei, and giant-cells—large granular masses filled with nuclei. Although these new cells are produced over the entire surface of the peritoneum, yet, as a rule, they are more numerous in little patches here and there. These little patches may be heaped together in such numbers as to form nodules visible to the naked eye. There is never any stroma between these cells.

This form of peritonitis occurs most frequently with organic heart disease, with cirrhosis of the liver, with chronic pulmonary phthisis, and with acute general tuberculosis. In the two latter diseases he thinks they have been improperly called tubercles.

He describes a form of chronic adhesion of peritoneal surfaces that occurs without the intervention of fibrin, but, as he supposes, by coalescence of the branching cells and a production from them of a fibrillated basement substance, the fibrils crossing in all directions. In the midst of these fibrils he finds the nuclei of these cells. He finds also in the immediate neighborhood of these adhesions thousands of branching cells that are attached one to another and float free in the water, the fixed end being attached to the peritoneum. He regards such a peritonitis with adhesions as a more advanced stage of the forms of cellular peritonitis already described, and the new cells are changed into membrane.

Sayre has published an extraordinary case in the Transactions of the Pathological Society. He calls it chronic proliferative peritonitis; it might be called more aptly the consequence of peritonitis.

A large, strong man fell from a hammock, the rope breaking, upon his shoulders, and felt a severe pain in his stomach, and soon developed symptoms of peritonitis. This pain never entirely subsided. The peritonitis was recognized. About one month after he was tapped, and 240 ounces of serum were drawn. He was tapped one hundred and eighty-seven times, and 1203⁵/16 pounds of fluid were taken from him during the remainder of his life. At post-mortem examination 3000 cc. of yellow serum were found. The liver and spleen were covered by a thick layer of false membrane, intestines were glued together in the upper part of the abdomen, and the stomach was adherent to the lower surface of the liver. The portal vein was contracted by this membranous coating. There were numerous other lesions in the heart and pleura, but these will account for the dropsy.

This man was unusually strong and hearty until 1876, when he had an attack of double pleuro-pneumonia, and in 1878 he slipped on the front steps and fell, but seemed to recover from the effects of this. The fall from the swing occurred in July, 1879. He died in February, 1884.¹⁰

¹⁰ Med. Record, April 19, 1884.

Tubercular Peritonitis.

This form of disease is by no means uniform in its first symptoms or in its progress. The only things uniformly attending it are tubercles on the peritoneum and more or less of inflammatory effusion, chiefly lymph and serum; tumor and hardness of the bowels, general or local; deranged function of the stomach and intestines; emaciation; and extreme fatality.

In some cases the invasion is acute and marked—a chill followed by fever, vomiting, early development of meteorism, and in a few days a point or points of resistance to pressure, but not necessarily dulness on percussion. In a few days the febrile action and the meteorism may subside, leaving the symptoms of local peritonitis. But we have not long to wait for a renewal of them and an evident extension of the inflammatory action. Remission and relapse alternate at varying intervals, until the whole extent of the peritoneal surface seems to be involved in inflammation. With this mode of development meteorism may not be renewed in the most common way. The lymphy product of inflammation may so bind the intestines to the posterior walls of the abdomen that they cannot extend forward, but are pushed upward against the liver and diaphragm, and so encroach on the thoracic space. But then the anterior parietes are tense and hard, and do not move in respiration. The febrile heat may not continue more than two or three months, but the pulse will be frequent to the end. There will be a thinning of bowel walls, and here and there a knuckle of adherent intestines may cause some prominence and give some resonance on percussion. There will be also occasional vomiting, and the dejections will be irregular—maybe only deficient or thin; there may be an alternation of constipation and diarrhoea.

Tuberculous ulcerations of the mucous layer of the bowels is not uncommon in tubercular peritonitis, and these ulcers have in rare cases perforated and allowed the fecal matter to accumulate in considerable quantity in a sac limited by previous adhesions. In all forms of tubercular peritonitis death is caused as often by grave complications as by what appears to be the primary disease. The affection occurs in probably every instance in those who had at the beginning, or had acquired in its progress, what we call the tubercular diathesis. We are not surprised, therefore, to find on inspection a wide diffusion of tubercles in the body, particularly on other serous membranes, and in the lungs. Death may occur, then, from phthisis pulmonalis or from pleurisy or meningitis, as well as from the exhaustion and accidents of the peritoneal disease. The effusion serum or turbid serum is very common in tubercular peritonitis, and can be recognized by the dulness it produces in part of the cavity, and sometimes by fluctuation. It is often sacculated, but it is not constantly found after death, it having been absorbed before, and perhaps long before, that event.

In other cases the invasion of the disease is stealthy and deceiving. It comes so quietly that the patient is not conscious of any local disorder beyond a dyspepsia and irregular action of the bowels. He has a pulse of growing frequency, but if he knows it he ascribes it to his dyspepsia. He is slowly losing flesh and strength; this he accounts for in the same way. At length a perceptible swelling of the bowels attracts his attention. At this stage the physician finds that the swollen bowels are tympanitic everywhere or only in the upper, while there is evidence of fluid effusion in the more depending, parts. He discovers some, it may be little, tenderness on pressure, and a pulse of 85, or maybe 90, increasing in frequency toward evening. The appetite is poor, the digestion slow, and occasionally there is vomiting; the complexion is pale and a little dingy; the skin of the abdomen may be dry and rough or may be natural; some colicky pains have been or soon will be felt. From this point the disease gradually advances. The distension of the bowels slowly increases or they are firmly retracted; the emaciation increases; the strength diminishes; there is often cough, which is generally dry; the bowels are slow or diarrhoea alternates with constipation; with the distended bowels there is always more than natural resonance on percussion, except when there is fluid effusion, though not often the full tympanitic sound observed in acute diffuse peritonitis. This resonance is not equal, always, in different parts of the abdomen; the respiration is embarrassed and almost wholly thoracic. The abdomen is often as large as that of a female at full term of pregnancy, and indeed the condition has been mistaken for pregnancy. This is an inexcusable blunder in a case like that which I have in mind—a young unmarried woman. She had no dulness on percussion in the space that would be occupied by the gravid uterus, but rather resonance. The case might have been a little less clear if there had been fluid effusion in the abdominal cavity, but if this were not encysted it would flow from one side of the abdomen to the other when the patient turned correspondingly in bed; if it was encysted, there would be small chances that it would have the shape and position of the gravid uterus; if it had, there would be no chance of hearing in it the foetal heart or feeling the foetal movements; and after all this there remains the experimentum crucis—a vaginal examination.

At first the diagnosis is unavoidably uncertain. Some aid is found, possibly, in the medical history of the family, in tuberculous antecedents, yet I remember cases in which no phthisis could be found in any living or dead member of the family on the paternal or maternal side as far back as it could be traced. Some aid is found if the patient himself has any of the physical or rational indications of pulmonary phthisis, and yet there are recorded cases in which the abdominal symptoms were the first to appear. The prominent German physicians attach great importance to the pre-existence of a cheesy mass or degeneration somewhere in the body as the real parent of tubercles wherever they appear. The truth of this doctrine, I do not think, has received anything like universal recognition; and if it had, as this cheesy degeneration is often, perhaps commonly, only discoverable after death, it could rarely give any assistance in diagnosis, so that the early diagnosis is always difficult, and a very early one often impossible. But as time goes on, and the symptoms are better defined and show themselves one after another as they are above described, it seems as if a careful observer could not confound it with anything except perhaps one of the other forms of chronic peritonitis or cancerous peritonitis. As to the latter, the cough which exists in most cases of tubercular peritonitis will assist in the distinction, but a physical examination much more; for a cough does not always attend phthisis when this disease exists; for example, I visited a daughter of one of the distinguished gentlemen of Vermont. She had had the bowel symptoms that indicated tubercular peritonitis for eight or ten months, and the diagnosis was not difficult. Remembering Louis's opinion that if tubercles invade any other part of the body, they are likely to be found at the same time in the lungs and in a more advanced condition, I examined the lungs, and found in the upper part of the right a cavity so large that it could have received a fist. I was only surprised by the fact that she did not cough, and had not coughed. She herself assured me of that (she was twenty-one years old); her physician, who was present at the visit, had never heard her cough, and had no suspicion of any pulmonary complication; but, more than all, her mother, who had walked with her, slept with her, eaten with her, travelled with her, and from the beginning of the illness had not been out of her company more than twenty minutes in any twenty-four hours since the disease began, had never heard her cough. Here, then, the nervous deviation to the abdomen, or whatever else it may have been, had so benumbed the sensibility of the pulmonary nerves that the alarm-bell of phthisis had never been sounded; but the cavity, had there been any doubt whether the bowel disease was cancerous or tuberculous, would have almost fully settled the question. But more of the peculiarities of cancerous peritonitis a little farther on.

The lesions of this disease (or its pathological anatomy) differ considerably, but the differences are in the amount of tuberculous deposit and the secondary results, not in the real nature of the disease. Lebert has published among his plates of pathological anatomy one which shows the peritoneum thickly sprinkled over with small tuberculous grains, and represents each particular grain surrounded by a little zone of inflammatory injection. There is yet no exudation, but that would soon follow. A fibrinous exudation will soon come over this primary deposit, and undergo a kind of organization, or at least get blood-vessels, which in their turn can furnish the material for a new crop of tubercles. These again provoke a new layer of fibrous tissue, which also becomes studded with tubercles, and so on, till a thick covering is formed over the intestines. But the same material is interposed between their folds, separating one from another and compressing them and diminishing their calibre; at the same time this agglomerated mass is firmly adherent to the abdominal walls everywhere. The new material may have a thickness of half an inch or even more. I remember how surprised and confused I was when I made my first inspection of such a case. The abdominal walls were cut through, but they could not be lifted from the intestines, but were firmly adherent to something. They were carefully dissected off and the bowel cavity (?) exposed; there was apparently an immense tumor filling the whole space: no intestines, no viscera, could be seen. A section was made through this mass from above downward, and another parallel with it and an inch distant from it, and this part removed. It appeared like a large, hard tumor, through which the intestine made several perforations. The new material appeared to be fibrous, with grayish-white tubercles sprinkled in through it everywhere, and pretty abundantly. In another case this fibro-tubercular material may occupy one part of the abdomen, and a large serous cyst or serous cysts another. The tuberculo-fibrous material may be found in markedly less quantity than is so far described, till there will be no more than in a case from Ziemssen's clinique, quoted by Bauer: "In the peritoneal cavity about four liters of yellowish-brown, slightly turbid fluid. Omentum thickened, stretched, adherent to the anterior wall of the abdomen and beset with hemorrhages; the same was true of the parietal peritoneum; between the hemorrhages whitish-yellow and entirely white tubercles occur, varying in size from the head of a pin to a lentil. The intestinal serous membrane was similarly invaded. The intestines intensely inflated; a number of ulcers on the mucous membrane, one approaching perforation. Covering of the liver thickened by fibrinous deposition."

The lungs and serous membranes generally will, in all probability, show more or less of tubercular deposit, the pericardium less frequently than the others.

The result in this affection, after it is fully established, is believed to be uniformly fatal, and at its commencement the difficulty of diagnosis may lead one to doubt whether his apparent success is anything better than apparent. Still, a plan which I have relied on is, I believe, worth announcing. As soon as the disease is recognized the patient is put upon the use of the iodide of potassium and the iodide of iron, in full average doses, and a solution of iodine in olive oil is applied to the whole surface of the abdomen by such gentle friction as will produce no pain; and after a minute or two of such friction the oil is brushed thinly over the surface and the whole covered with oiled silk. This dressing is repeated twice a day. The quantity of iodine to an ounce of oil will vary considerably in different persons; for some, seven to ten grains will be enough; for others, thirty will be needed. The iron is to make the application moderately irritating, and if it produce pinhead blisters or blisters a little larger, all the better. When the application becomes painful the oil is washed off, and the application is not renewed for two or three days. In this manner it may be continued for two or three months. Meantime, the patient is put upon the diet and regimen of the consumptive, the appetite encouraged; he takes sustaining food, with plenty of milk and cream, or cod-liver oil, as much fresh air as possible, and friction is applied to other parts of the body with dry flannel.

Cancerous Peritonitis.

Benign tumors of the abdomen are not frequently the cause of general peritonitis, and when they are, the grade of the disease is acute rather than chronic. They very often provoke local inflammation and become adherent to the neighboring structures. The same is true of malignant growths in the abdominal cavity, except that the adhesions are earlier formed and more likely to occur. Localized cancer, of whatever variety, is not very prone to produce general peritonitis, even though there be multiple developments of it. But when the disease takes the disseminated form, and is sprinkled over the whole extent of the peritoneum, then inflammation is almost certain to occur—not of high grade, and yet deserving the name subacute rather than chronic. A case which illustrates this statement has come under my observation within the last year. I will recite it with sufficient detail to make it intelligible.

A lady about forty years of age had, up to the summer of 1881, enjoyed very good health, though she was never robust. At that time she felt her strength abating and her stomach disordered. She sought health in various places, and took professional advice in September. It availed her little; the bowels were gradually swelling and fluctuation could be felt. She was losing strength and flesh. There was not a cachectic countenance, but the features were growing sharp. She had suffered but little from pain till October. At that time she was at the family country home. Then she began to suffer from a severe pain in the left thigh; and this, it was noticed, increased as the accumulation in the bowels increased, and at length her physician felt compelled to tap her—not so much on account of great distension of the bowel as in the hope of relieving the pain. He drew off nine quarts of gluey, viscid fluid, and her pain was wholly relieved. Twelve or fifteen days after this she was brought to her city home, and her city physician, seeing that her case was a grave one, sought the aid of a distinguished gynæcologist. She was then again tapped to give him a more satisfactory examination. He found the ovaries considerably enlarged and hard. They could not, however, be felt by pressing the fingers into the pelvis from above—only by the vagina. I saw her on the 10th of November. The fluid had again made considerable tumefaction of the bowels, and she was again suffering great pain in the region of the right kidney and in the leg of the same side, together with cramps. The relief given by the first tapping induced us to propose its repetition. It was, however, delayed till the 14th, that the physician who had tapped her before might be present and assist. The quantity of water drawn was again nine quarts, and again the pains and spasms were quieted. The examination of the abdominal fluid was interesting. It was nearly clear, reddish, of syrupy flow and consistence, and so viscid that while a portion of it had remained on the slide of the microscope long enough for the examination of its constituents the thin cover became so firmly attached to the slide that it could not be removed without breaking or long maceration. The albumen was so abundant that the fluid was completely consolidated on boiling. Fibrinous threads were running through it in great numbers, and here and there was a cell of large size, round, granular, but not plumped up with granules, with a nucleus barely less in size than the cell itself; its outer border within, but only just within, the boundary or wall of the cell. It was the nucleus that was granular, for there was little room for granules between the nucleus and the cell wall. The vial containing the fluid had been standing three or four hours for a sediment. This in a vial four inches high occupied the lower half, and gave nothing to the dropping-tube till the sedimentary matter was drawn into it by suction. This matter consisted of fibrillated fibrin in large quantity; a great number of the cells just described, some grouped, but most separate or single. There were pus-cells in moderate quantity, each having the amoeboid movements, and a considerable number of red blood-corpuscles, some of natural form, some crenate.

Immediately after the tapping the flaccid condition of the abdominal walls admitted an examination. A solid, hard mass was found running across the upper part of the bowels, a nodule of which was lying on the stomach at the point of the ensiform cartilage. A harder mass of irregular shape was also found just above the pelvis on the right side, extending upward and to the right. This was in extent two by three inches. The ovary, however, could not be detected by pressure from above downward. The diagnosis up to this time was hardly doubtful, but these revelations made it complete, and crushed any lingering hope of the patient's recovery.

While the pain and spasm ceased after the tapping, the oedema of the left leg, which came on some time before the last tapping, did not diminish. The hard spot near the right iliac fossa was tender on pressure, but otherwise hardly painful. While the fluid did not exceed six quarts or so, she had little pain anywhere. There were no external glandular swellings. Her appetite was poor, and she took but little food. She vomited very little till the end was approaching. The urine contained a few globules of pus, some pigment matter, two or three hyaline casts, but no trace of albumen. For sixteen days following November 14th the patient was comfortable, but the fluid was slowly filling the bowels again. At that time the pains already referred to began to return. On December 5th they required another tapping, and preparations were made for it, but vomiting, rather severe, led to its postponement to the next day. The quantity of fluid drawn was nine and a half quarts. It was of the same syrupy consistence as that previously drawn, and under the microscope showed exactly the same constituents and gave the same quantity of albumen. The next day stercoraceous vomiting commenced, with no movement of the bowels, except what was produced by 10 grains of calomel given on the second day of this vomiting. That acted well and produced a temporary relief. She after this took no food by the mouth, but milk and beef-tea were injected into the rectum. Still, the fecal vomiting returned, and she died on the 15th.

The post-mortem examination was made on the 17th by William H. Welch. I could not attend it. His report is complete as to the main features of the case, though it does not furnish an explanation of the spasms and the oedema of the left leg, regarding which Welch was not informed. The pain and spasm were doubtless due to backward pressure of a diseased part on a nerve or nerves, and the oedema to a narrowing of the iliac vein by pressure or constriction by fibro-cancerous matter on its outer sides. "The peritoneal cavity," he says, "contained somewhat over a gallon of clear, yellow serum. Both the visceral and parietal layers of the peritoneum were thickened, in some places more than in others; this was especially marked on the anterior of the stomach and on the lower part of the ileum and in the left iliac region. The omentum was greatly thickened and retracted into a firm mass (or roll), which extended somewhat obliquely across the body, more to the left than to the right. The mesentery was much thickened and contracted, drawing the intestines backward. In a few places only was the peritoneal surface coated with fibrin, and the intestines were mostly free from adhesions. The coils of the lower part of the ileum, however, were firmly matted together by organized connective tissue in such a way that they were twisted, often at a sharp angle, so as greatly to constrict the calibre of the gut. The serous and muscular layers of the intestine at this point were greatly thickened. By these causes there appeared to be a complete obstruction at a point about six inches above the ileo-cæcal valve. By careful dissection these coils were straightened out, so as to remove the main cause of obstruction. The peritoneal covering of the liver was adherent to the parietal layer.

"The surface of both the visceral and parietal peritoneum was studded over with hundreds of small, firm, whitish nodules, generally not larger than a pea, and often not larger than a pin's head. In some places they had coalesced and made firm patches an inch in extent. This same material was found in the contracted omentum in considerable quantity. In a few places, particularly on the uterus, a blackish pigmented deposit appeared.

"The ovaries were not adherent, but both were enlarged to the size of a hen's egg. The outer surface of each was rough and corrugated. The new growth was deposited on the exterior and penetrated each a quarter to half an inch. It was of uniform white color and of firm consistence.

"The stomach wall was thickened nearly throughout its extent, but particularly in the anterior part, where it amounted to thrice the normal thickness. This consisted wholly of hypertrophy of the muscular coat and increase of fibrous tissue in the peritoneal layer. This new growth was traced, in the interlacing bands, from the surface into the muscular coat. In the outer layer of the stomach were found three small white nodules. The mucous membrane of the organ was healthy or a little pale.

"The retro-peritoneal glands along the aorta were enlarged, soft, and of a reddish-gray color. A nodule was found in the wall of the duodenum outside the mucous membrane, and one in the Fallopian tube."

Every organ in the abdomen and chest was examined, but nothing important found except what is here recorded. Welch concludes his record with the following diagnosis: "Primary scirrhous carcinoma of the ovaries. Secondary deposits in the peritoneum, in the outer layer of the right Fallopian tube, of the stomach and duodenum, and in the retro-peritoneal glands. Chronic peritonitis, intestinal obstruction."

This case presents to the reader so accurately the usual course of cancerous peritonitis, and the inspection its lesions, that a treatise on the subject is hardly called for. It often happens that cancerous antecedents in the patient or his relatives will lend an aid to the diagnosis, which this case did not present. To distinguish this disease from tubercular peritonitis no question can arise except in its dropsical form, and then the lungs in every case of the latter that I have met with have the physical signs of tubercles, though not always the rational indications. The pulse is much more accelerated in the tuberculous variety. I omitted to state that the temperature of this patient was often taken, and till the closing scene was never found more than one or two degrees above the healthy standard, and the morning and evening heat did not materially vary; the opposite of both, then, would be expected in a tuberculous case. The existence of meteorism is much more common in the tubercular disease; indeed, in the cancerous case recited there was none of it. The duration of the two is different—that of the cancerous kind is recorded in months, while the tuberculous variety may continue two years. The cancerous is more likely to be attended by alarming accidents, like the complete obstruction of the bowels, large hemorrhages, and a sudden lighting up of acute peritonitis. Finally, in the light of the case here recorded, it seems probable that the examination of the abdominal fluid will become of great importance. I have never carefully examined the fluid of tubercular dropsy, but it does not seem probable that it will have the syrupy appearance, the large amount of albumen, the abundance of fibrin-fibres, and the granular large cells with nuclei only perceptibly less in size than the cells themselves, that were repeatedly found in this case—found by two observers, and at every tapping after the first.

TREATMENT cannot be curative; it therefore consists of such administrations as will relieve pain, give sleep, improve the appetite, increase the flow of urine if it be scanty, and relieve the bowels if there is a tendency to constipation. It is as much the duty of the physician to put off the fatal day, when he can, in incurable affections as it is to cure those that will yield to his prescription and advice. In the case just narrated opium or an opiate alone produced such unpleasant after-effects that she was unwilling to take it, but when the extract of belladonna was given with it she slept pleasantly, and could take her food the next day.

Infantile Peritonitis, or Peritonitis of Childhood.

Bauer, in Ziemssen's Cyclopædia of Practice of Medicine, and Wardell, in Reynolds's System of Medicine, have each devoted a chapter to this form of disease. They refer to the fact that the foetus may have peritonitis before birth or be born with it, or may have it when a few days old. They say that this form of the disease occurs most frequently in lying-in asylums or foundling hospitals, and that it has been supposed to depend on a syphilitic taint. They say, too, that it follows erysipelas, scarlet fever, measles, etc. I do not perceive that the description of either of these authors makes any marked distinction between this and the same disease in adults, except what may arise from the inability of the infant to describe its sensations, and the more rapid course of the disease to a fatal result—in some cases twenty-four hours. Having myself had no obstetrical practice, or next to none, I have nothing to add to their statements, and can from my own knowledge abate nothing. I therefore refer the reader to these chapters, and to the references given by the first of these authors, for a fuller knowledge of the matter.

Regarding the comparative exemption of children, after the first few weeks of life, from spontaneous peritonitis, referred to by one of these authors, I can fully confirm his statement. Though I have assisted in the treatment of many children suffering from peritonitis, I have difficulty in recalling to mind a single case in which the disease was not caused by perforation of the intestine or vermiform appendix of the cæcum, and in much the greatest frequency perforation of the appendix.

B. F. Dawson,¹¹ after reciting a case in which the liver had undergone a peculiar degeneration and was attended by peritonitis before birth, states that Sir J. Y. Simpson observed nine cases in his own practice "and notes more than a dozen from different sources." These cases seemed to have been caused by the ill-health of the mother during gestation, or excessive labor, injuries, venereal disease, and were mostly attended by grave disease; the viscera often, the liver; but sometimes the mother was perfectly healthy, and the peritonitis was the primary disease. Death almost always occurred in utero or shortly after birth. In one instance the child recovered.

¹¹ N.Y. Med. Journ., Dec., 1882.

The Med. Record takes the following from Schmidt's Jahrbucher for Jan. 7, 1883: "Dr. Oscar Silbermann recognizes two varieties of peritonitis in the new-born. The non-septic or chronic is developed usually in the first third of foetal life, and is generally syphilitic in origin. If the peritoneum covering the intestines be involved, as well as that over the liver and spleen, various forms of intestinal obstruction may result. Most frequently there is occlusion of the anus, less often stenosis or complete stricture of the small intestine. Of a number of cases of congenital occlusion of the intestine collected by the author, all ended fatally, only one living beyond twelve days.

"The second, acute or septic, form of peritonitis in the new-born the author divides into two varieties, according as the peritonitis is only a part of general infection or is the sole manifestation of the septic poison. In either case the point of entrance of the poison is always the navel wound. The symptoms, which need not all be present in a given case, are vomiting, watery stools, meteorism, ascites, abdominal tenderness, icterus, etc. The pulse and temperature may vary in degree in different cases. A cure of the septic form is possible; therefore the treatment should be carefully considered. The navel wound should be cleansed, and the child is to be isolated from its mother. To control the fever quinine may be given. Priessnitz's sheet is of value; vomiting may be checked by chloral (one-half to one grain in water). The strength should of course be maintained by stimulants if necessary."

Ascites.

The accumulation of fluid indicated by this name has already been referred to in its relations to several causes. There are, however, conditions producing it which have not been considered or only considered partially.

The most prolific source of abdominal dropsy is obstruction of the portal circulation on its way to or through the liver. Condensation of the liver structure in cirrhosis, with destruction of many of the portal capillaries and compression of many more, is prominent in this connection. The compression of the liver caused by an adventitious external covering, referred to under the head of Local Peritonitis, acts similarly, whether it compresses the vein at its entrance into the liver or not, although it is not known to produce any destruction of the portal capillaries. Some enlargements of the organ are attended by the same result, but they are always associated with a hardening of its structure. The disease lately called waxy liver, now often denominated lardaceous, belongs to this class, as does that condition in which the organ is enlarged, hardened, and fissured, regarded as syphilitic liver. That both these diseases may have a syphilitic and mercurial origin is not a point now under consideration. They both harden the hepatic structure and obstruct the portal circulation, while they may not in equal degree hinder the progress of arterial blood. This is explained when we remember the diminished force that propels the portal blood. Neither of these diseases produces dropsy early in its progress, but, as I have seen it, always before it reaches its fatal termination. Fatty liver has not, in my observation, produced dropsy, although I have seen livers made very large by that disease, and the absence of dropsy when the liver has been large has aided me in distinguishing it from the waxy disease. Cancer of the liver in some instances does, and in others does not, produce dropsy of the bowels. It is only certain to have this result when a tumor is in position to press upon and obstruct the portal. Hypertrophy of the liver, caused by mitral regurgitation or other disease of the heart, does not generally produce dropsy, but, aided by anæmia or watery condition of the blood, such a result is possible. In children, however, it is not very rare to see the bowels distended by dropsy, and to discover that the liver is enlarged at the same time. It is common in such cases that the dropsy and the hypertrophy disappear after a few weeks of treatment. This may occur in a child that is anæmic, but without any disease of the heart. Such a case was brought to me two or three months ago, and after four weeks of treatment by tonics and diuretics the health was re-established. There is one point in these cases of some importance. When the child lies on his back, if the abdomen is much distended, the liver cannot be felt. It has sunk away into the fluid, and in this position ordinary percussion cannot ascertain its dimensions. In the July number (1840) of a quarterly journal edited by Swett and Watson, I published an article in which I reported the conjoined labors of the late Camman and myself on a new method of combining auscultation and percussion, with its results, under the heading "Auscultatory Percussion." By the method described in that article—viz. by placing a solid stethoscope, or for that Laennec's first stethoscope, a rolled-up pamphlet, on the chest at a point where the liver has not fallen away from its walls, and percussing on the abdomen from below upward—a point is reached whence the percussion sound is brought sharply to the ear, while half an inch below the sound is dull and distant. The lower edge of the liver is thus easily recognized, and its upper boundary is found in a similar manner or by ordinary percussion, so the difficulty of measurement disappears.

In such case, when the dropsy disappears and the liver recovers its natural dimensions at the same time, the inference is that the hypertrophy caused the dropsy, and that the hypertrophy was of the kind called simple. The nutmeg liver is thought to have an agency in producing dropsy, but as it is for the most part associated with diseases that have been called dropsy-producing, its bearing on this effusion may yet be regarded as uncertain.

It is common to speak of heart dropsy in such a way as to imply that disease of the heart alone can produce abdominal effusion. I doubt it. I even doubt whether the heart alone can cause the anasarca that is so often attributed to it. In following a great multitude of heart diseases from the time they were recognized to their termination, I have been struck with the ease with which the patients attend to their business, sometimes even laborious business, for years—in one instance fifty years—with almost no complaint, and how rapidly their condition changes as soon as albumen and casts appear in the urine. I have been compelled by these observations to ascribe the anasarca and oedema that makes this last stage of heart disease so distressing to the kidneys, and not to the heart. Double pleuritic effusion is not uncommon under these circumstances, but every physician must have noticed the rareness of troublesome abdominal dropsy, while there is sometimes—perhaps often—a little effusion; and when in the exceptional cases there has been much, it was almost always accounted for by a dropsy-producing change in the abdominal organs, not, perhaps, discovered during life; so that for me, while they produce overwhelming effusions in other parts of the system, they are minor agents in the production of ascites. Phthisis is occasionally attended, toward its close, by oedematous legs and albuminous urine, but I cannot report any important relation between these and peritoneal effusion. I can say the same of chronic bronchitis. I record this negative testimony regarding the two last-named diseases, because I find them enumerated among the causes of abdominal dropsy.

Cancer may invade the portal vein, tumors of adjacent parts other than those of the liver, or an aneurism may compress it and cause dropsy. Hydatid tumors may do this. Diseases of the pelvic organs, both acute and chronic, may produce it, but then the disease would fall into the class of those produced by chronic or subacute peritonitis.

DaCosta thinks he has lately had a case of chronic peritonitis attended by ascites. It was in a woman thirty years of age, who had been thrown with force upon the frame of an iron bedstead, striking the lower part of the bowels. Pain and tenderness followed. These were not confined to the injured part, but extended to the whole abdomen; and there was menorrhagia. After a time there was fluid effusion in the peritoneal cavity, which slowly increased till her state demanded relief from tapping. The fluid after this operation did not return. The pain and tenderness were constant symptoms all through. She slowly improved, and at the time the case was reported it was believed that she would soon be discharged from the hospital. The only doubt which DaCosta finds regarding the diagnosis is in the facts that the liver was diminished in size and that the spleen was moderately enlarged, and he admits the possibility that an adventitious capsule of the liver may have caused the ascites, but believes that it was dependent on chronic peritonitis.

Acute peritonitis subsiding into chronic, with increase of fluid effusion, as I have already said, I am not familiar with. That occurring in cancerous and tuberculous peritonitis has already been considered. But in relation to these some facts regarding frequency of occurrence, collected by Bristowe, are worth quoting. He says that in 48 cases of tubercular peritonitis, dropsy was found in 12, and that in 22 of peritoneal cancer, 12 had more or less ascites. He further adds, regarding cirrhosis, that of 46 cases observed post-mortem, there was dropsy in only 20. This is not surprising, as in all the diseased conditions of the liver that produce dropsy the anatomical changes must reach the point at which there is considerable portal obstruction before the effusion will occur.

The amount of fluid found in ascites varies greatly. In some it may remain for a long time stationary at four or five quarts; in others the suffering caused by an accumulation of nine or ten quarts will demand its removal; and in a few cases twenty quarts have been removed in one operation. It is in cirrhosis that the largest quantity is found, and it is in this disease and in cancerous peritonitis that the most frequent tappings are required. The quality of the fluid also varies markedly: from being almost as clear and thin as spring-water it may be almost ropy, or in color greenish or yellowish or slightly red; it is very likely to contain albumen; and it is probable that a further study of its microscopic elements may enable us to resolve doubts regarding the cause of the effusion. It very often contains blood-corpuscles.

Bristowe finds from hospital records that ascites occurs in about equal frequency in males and females, but, as everybody has noticed, that hepatic dropsy is much more frequent in men than in women. Ascites, he says, is most frequent between the ages of thirty and fifty, and next between twenty and thirty and between fifty and sixty, but is not uncommon above the latter age; and it occurs in children.

SYMPTOMS.—In general, ascites is easily recognized by the swollen state of the bowels: a well-rounded swelling when the patient stands or sits, but spread out in the flanks when he lies on his back; the fulness of the side on which the patient may be lying, and the flattened condition of the opposite side,—belong to this disease, and as a group to no other. The results of percussion are significant in the movement it causes in the fluid, and for the resonance or flatness it produces. When the patient lies on his back, tapping with the finger-ends on one side of the abdomen sends a wave of the fluid across to the other side, where it is perceived as a gentle blow by the applied fingers of the other hand. If the abdomen is not full, this wave will be produced at the upper level of the fluid, but not above that. If this wave cannot be sent across the body, it may be found on either side by percussing above and feeling for it below; percussion also teaches where the fluid is, and where it is not, by the dull sound it produces. It is rare in ascites that the intestines do not float on the surface of the fluid, at least from the umbilicus upward, and there give a loud percussion sound, while toward the back, and often toward the pelvis, it is dull, or even flat; changing the position of the body, the resonance will be uppermost and the dulness in the most dependent part. Then the softness or impressibility of the abdomen till the tension becomes great is noticeable. The changed position of the fluid as the body is turned from side to side is important. A very small quantity of fluid can be detected in this manner. The patient is placed on his right side and percussion is made in the right flank: there is dulness, while in the left flank there is resonance. The patient turns on to the left side: dulness now changes position, and is on the left, and on the right resonance. If it is feared that some undetected fluid remains in the pelvic cavity, the pelvis may be raised by pillows and the same examination repeated, or he may be placed in the knee-and-elbow position referred to by Bristowe, and the percussion will then be made upward in the umbilical region. In some cases the contraction of the mesentery will not allow the intestines to rise through a large amount of fluid and float on it; but such cases are almost confined to the cancerous and the tuberculous varieties of the disease; and as in these the symptoms are grave, the physician will probably have visited his patient many times before this contraction will embarrass him. Besides, when mesenteric contraction occurs there is a very strong probability that the omentum will also be contracted, be rolled up, and lumpy; as this can almost always be felt above the level of the umbilicus, he has in it an explanation of the absence of resonance on the fluid. It has happened that oedema of the abdominal walls or fatty accumulations there have given a delusive though feeble fluctuation on percussion. In such cases, if the patient make moderate pressure with the back of a small book in the course of the median line, that kind of wave will be broken, while a wave in the abdominal cavity will not be prevented. When there is considerable distension of the abdomen by fluid, weak spots in the abdominal wall often yield and make a tumor. This is very common at the umbilicus, where a little bladder is lifted half an inch or more above the general curve of the abdomen. The fluid frequently follows the track of hernias. In females it has been known to press the anterior wall of the vagina backward and downward, so as to make it protrude at the vulva. It has, in one of my own cases, by downward pressure caused complete prolapse of the uterus. It is very often attended by oedema of the lower limbs. This is accounted for by the pressure of the abdominal fluid on the veins that return the blood from these parts, or in cirrhosis by contraction of the ring or notch through which the vena cava passes in the liver. If there is general oedema, the cause will probably be found in disease of the kidneys; or if in one limb, in pressure or thrombosis of one iliac vein. As the disease advances the accumulating fluid forces the diaphragm upward, diminishes the breathing room, and threatens the life still more. Then the patient cannot lie down in bed, but spends his nights as well as days in an easy-chair, and sleeps leaning forward on a support for his forehead. The veins on the abdominal surface will fix attention. With almost any large tumor in the cavity they become more or less enlarged. But in cirrhotic dropsy this becomes more striking than in any other affection. The enlargement is attended by a reversion of the blood-current on the lower half of the abdomen. This is early shown by emptying an inch or two of a vein with the finger, drawing it either upward or downward, and noticing from which direction it is refilled when the pressure is removed. The pelvic veins do not readily discharge their blood by the natural channels, and by anastomosing branches it is forced over the surface of the abdomen and into the thoracic veins, these latter becoming in turn greatly enlarged. The appetite is commonly poor, the digestion flatulent, the pulse accelerated. Emaciation is gradual or rapid. The urine is commonly scanty, and in cirrhosis of a reddish hue. The skin is apt to be dry, particularly so in simple chronic peritonitis. The tongue has no characteristic fur, and is often, almost always toward the close, dry. The mind is not affected till near the end; then often the patient is delirious, commonly mildly. Diarrhoea is not uncommon, and even dysentery has been observed. The result is almost always unfavorable, or, as has been said, lethal.

The diagnosis is not often difficult. When, as in chronic peritonitis and in tuberculous peritonitis, the fluid is confined in a sac or sacs, each particular pool will be yielding to pressure, but elastic, and will give the percussion wave, though it may extend but a short distance. To distinguish ovarian dropsy—ovarian cysts, as it is now called—from ascites may require a few words. Ovarian tumors of all kinds are found to be more prominent on one side when they rise from the pelvis than on the other. This is not the case with ascites. The uterus and its appendages lie in front of the pelvic intestine, and when any of them ascend above the pelvis they must occupy the same relative position. In other words, a large ovarian cyst must lie in front of the intestines, while intestinal resonance should be found behind and in the sides. But if the ovarian cyst does not occupy the whole height of the bowels, intestinal resonance may exist above it, and the dulness may be found below, bounded by a portion of a circle, and sometimes the cyst walls are resisting enough to allow its boundaries to be ascertained by the fingers. This cyst can also be felt in the vagina; and the uterus, instead of being pressed down, is sometimes lifted upward, so that it cannot be reached in the vagina, but can be felt through the abdominal walls just above the pelvic bones. A condition more troublesome than this is when ovarian cyst and ascites occur together. Then the posterior or lateral resonance is lost when the patient lies on her back, but can be found on one side when she lies on the other. In that concurrence, in dorsal decubitus it is possible by pressure or a little blow to send a wave of the ascitic fluid over the front of the cyst. This can be seen as well as felt. Should the patient take the knee-and-elbow position, the intestinal resonance may be restored in both flanks.

TREATMENT.—In opening the chapter on the treatment of ascites it is usually said, Give principal consideration to the diseased conditions that have caused the dropsy; in other words, cure cirrhosis, cancerous peritonitis, tubercular peritonitis, heart disease, and the secondary affections of the abdominal organs, release the liver from the dangerous compression to which it is subjected, and all will go well. But they do not inform us how these impossibilities—at least in most cases impossibilities—are to be achieved. It is true that the physician would not shrink hopelessly from the treatment of simple chronic peritonitis. But this is one of the rarest causes of ascites. A physician in a long lifetime may not have seen a case. It is true, ascites is a symptom, always a secondary, or even a tertiary, affection; and theoretically there can be no better advice, but practically it cannot amount to much. Then, if the cause cannot be removed, it remains to do our best to relieve the patient of his load and strive to prolong his life to its utmost possible limit. In doing this the physician will often find himself able to give gratifying relief, and once in a great while to rejoice in a cure.

The three great emunctories, the skin, the bowels, and the kidneys, are chiefly appealed to for relief in this as in other serous accumulations. Most physicians prefer to use the diuretics—first, because if they will act at all, they act so quietly and produce so little debility that whatever can be gained by them is obtained at small cost to the system. The form of ascites that most resists diuretics is that which originates in cirrhosis. Often a full trial of them, with suitable changes from time to time, is of no avail, yet now and then the kidneys yield to persuasion and act freely. The saline diuretics and digitalis are most in favor with some. In the early part of the present century a pill composed of squill and digitalis in powder, and calomel, each one grain, given three times a day, was almost universally chosen. In place of the calomel the blue mass was often preferred. When this prescription had produced a little ptyalism the mercurial was omitted and the squill and digitalis continued. It has often been observed in dropsies of all kinds that diuretics act better after a little mercurial action is set up in the system. The diuretic that I most frequently prescribe is made of the carbonate of potass. ounce ss and water ounce vj; to a tablespoonful of this a tablespoonful of fresh lemon-juice is added. This is taken every two hours, and at the same time a dessertspoonful of the infusion of digitalis or more is taken three times a day. This is an old prescription. Sometimes the old sal diureticus is used. This is the acetate of potassium. It is not always kindly received by the stomach. At Bellevue Hospital the following is much used: viz. infusion of digitalis, ounce iv; bitartrate of potash, ounce j; simple syrup, ounce ss; and water added to make a pint. This is taken pretty freely. But it would require many pages to exhaust the diuretics. I will only add that I have more confidence in the salts of potash and soda, singly or combined, aided by digitalis and a mercurial, than in any others.

The diaphoretics that are most efficient are warm water and steam. A foot-bath long continued and frequently repeated, the patient covered with blankets, and the water kept at 90° or warmer, are very effectual in producing perspiration. Bricks heated or hot water in bottles, or potatoes heated, and enveloped in damp cloths and laid alongside of the body and limbs, form an extemporaneous vapor-bath of considerable efficiency. A vapor-bath can be easily extemporized in the following way: Have a kitchen vessel furnished by the tinman with a cover which has an inch tube fitted to this and bent so as reach the floor six feet from the fire. The pot should have a capacity of a gallon or more, and should be kept boiling briskly. Meantime, the patient, in his night-dress, has a double blanket brought over his shoulders from behind, and another from before, and fastened. Now he takes a chair (wooden), under which the steam is delivered. The blanket from behind is kept off his body by the back of the chair, and the front one by his knees. The steam, shut in in this way, soon brings on a sweat, and when it is sufficiently active the front blanket is thrown off, and the patient wrapped in the rear one and put to bed, when the sweating can be regulated by blankets. This is better than what is called the alcohol sweat, for in that the patient is bathed in carbonic acid gas as well as heat. A patient is sometimes enveloped in a hot, wet blanket with good effect. Pilocarpine has come into use lately as a sudorific. I have witnessed its effects many times and can testify to its certainty as a sudorific; but it is too debilitating for common use. Digitalis has sometimes acted with extraordinary power in this way, but there are grave risks in administering large doses.

Among the cathartics that may be used in ascites, it has seemed to me that the milder hydragogues are safest. One ounce of Epsom salts with a drachm of the fluid extract of senna can be taken every second or third day for months, if need be, with little reduction of strength, and sometimes with an increase of it. I had charge of a young man in the hospital in whom cirrhosis was unquestionable, and dropsy at one time extreme, in whom the abdominal veins had made furrows that would receive the little finger, who was wholly relieved by a drastic dose of elaterium every second day. I saw him three years after his discharge, and then his health was good. Notwithstanding this, I prefer the milder medicines.

Bristowe has seen no cures from either sudorifics, diuretics, or purgatives. I have seen one or more from each of those agents, all cirrhotic. He "has seen cures occasionally from mercury, iodide and bromide of potash, copaiba, and a combination of fresh squills and crude mercury." I agree with him in his statement that counter-irritants are useless, making exception for chronic peritonitis and the early stage of the tubercular variety. He thinks quinia, iron, and cod-liver oil are useful.

Paracentesis in almost every case will at length become necessary, and the question comes whether it should be practised early or late. If it be delayed till the oppression of the breathing makes it imperative, the walls of the abdomen will be so stretched as to present little resistance to the reaccumulation of the fluid, and a second tapping will be required in fifteen to twenty-five days. A bandage is a poor substitute for muscular contraction. If, on the other hand, the fluid is withdrawn before the muscularity is not stretched out of the muscles, then accumulation will be less rapid and the patient will be spared the suffering which large accumulations cause. But tapping is not always an innocent operation. It is sometimes followed by acute peritonitis. By the early tapping this risk is oftener taken. Reginald Smith suggests the use of a small canula by which only ten or twenty ounces of the fluid can escape each hour. This mode, he thinks, removes the danger of syncope and makes the bandage needless.

Hemorrhagic Effusion

in the peritoneum is a topic on which there is little to be said. A primary effusion of this kind probably does not occur. In hæmatophilia, where the mucous membrane of the nose and wounds bleed dangerously, there is no record of spontaneous bleeding into the peritoneal cavity. The same thing can be said of that very rare disease which has been called bloody sweat. An unmarried lady applied to me fifteen years ago with this disorder. The blood would ooze out at hundreds of points on the inner face of the arm; these would run together and drop off the arm, or the same thing would occur on the chest and in the bend of the knee. This would continue for two or three minutes, and then cease of itself, but to recur in one or more, rarely several, places. For years this habit continued. There was no irregularity of the menses. I could find no visceral disease; there was no nose-bleed. She lost strength, but only moderately. This kind of bleeding continued for several years. She is now approaching fifty years of age, and for the last two or three years has had no recurrence of the bleeding. There was never anything in this case to lead to the suspicion of peritoneal or other serous hemorrhage. In the few similar cases on record there is the same absence of all evidence of internal bleeding.

It has already been said that a certain amount of blood, as shown by its corpuscles, is to be expected in cancerous ascites, and with less uniformity in tubercular ascites, and not unfrequently in hepatic dropsy, as well as in acute peritonitis. This may not deserve to be called hemorrhage, on account of the moderate quantity of blood that is effused; but aside from that which results from rupture of blood-vessels it is about the only kind of it with which we are familiar.

Scurvy, and conditions of the blood analogous to those produced by that disease, make it almost certain that if pleurisy or pericarditis occurs while these conditions exist, it will be hemorrhagic. I am not, personally, acquainted with a single instance in which peritonitis in this condition has occurred. Copeland, however, says that hemorrhage in peritonitis has been noticed by Broussais and others. The blood is mixed with the serum and stains the surface of the false membrane, as in hemorrhagic pleurisy and pericarditis, and the disease is of an asthenic type, "occurring in the hemorrhagic diathesis." "The symptoms are inflammatory from the beginning, and rapidly pass into those indicating great depression; the pulse becomes rapid, small, and soft, death quickly supervening, with convulsions, cold and damp extremities and surface," etc.

Copeland has himself not seen a case, and regards its occurrence as very rare. Delafield states that "Friedreich describes two cases occurring in patients with ascites who had been frequently tapped. He says that both the parietal and visceral peritoneum was covered with a continuous membrane of a diffuse, yellowish-brown color, mottled with small and large extravasations of blood. The membrane was thickest over the anterior abdominal wall. It could be separated into a number of layers. These layers were composed of blood-vessels, masses of pigment, branching cells, and fibrillated basement substance. In many places the extravasated blood was coagulated in the shape of round, hard, black nodules. The new membrane could be readily stripped off from the peritoneum, and there were no adhesions between the visceral and parietal portions of the peritoneum."

The erosions of abdominal cancer sometimes open vessels of considerable size, causing large hemorrhage into this cavity and sudden death.

When aneurisms of the abdominal aorta rupture, they sometimes flood the abdominal cavity; oftener they open into the structures under the peritoneum on the left side, and make a large flat tumor extending from the point of rupture downward to the brim of the pelvis, and even beyond it.

A gentleman whose health was usually good, thirty-five years of age, felt an unwonted exhaustion and feebleness creeping over him. His countenance became pale, his pulse rapid, growing smaller and smaller. It seemed certain that there was hemorrhage somewhere, but until it was noticed that the bowels were growing tumid and hard there was nothing to guide us to its seat. Even then we were left to conjecture regarding the bleeding vessel. This sinking continued for thirty-six hours. After death it was found that a small aneurism had been formed on one of the vessels of the omentum, not larger than a small walnut, and had ruptured by a very small opening, and that it was by this small opening that life had oozed away.

Bleedings from stabs and other wounds of the bowels, from lacerations of the liver, spleen, uterus, and sometimes of the kidneys, should be mentioned in this connection; but as they, for the most part, fall into the hands of the surgeons, this is not the place to give the details regarding them.